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Langer-Gould AM, Cepon-Robins TJ, Benn Torres J, Yeh EA, Gildner TE. Embodiment of structural racism and multiple sclerosis risk and outcomes in the USA. Nat Rev Neurol 2025:10.1038/s41582-025-01096-5. [PMID: 40425864 DOI: 10.1038/s41582-025-01096-5] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 04/28/2025] [Indexed: 05/29/2025]
Abstract
Disparities in the incidence, prevalence and outcomes of multiple sclerosis (MS) exist in the USA, often to the detriment of Black and Hispanic people. Despite the common misconception that MS is a disease of white people, the incidence is highest in Black people. Disability accumulates faster and at younger ages in Black and Hispanic people with MS than in their white counterparts, and MS-related mortality in early and mid-adulthood is highest in Black people. These differences are often erroneously interpreted as evidence of innate racial or ethnic variations. In this Perspective, we demonstrate how race and ethnicity - social constructs with a limited biological basis that are often assigned by systems of power - can influence biology through lived experiences, a phenomenon termed 'embodiment'. We review how downstream consequences of structural racism can lead to biological outcomes strongly associated with MS susceptibility, such as imbalanced immune system development, dysregulated immune responses to the Epstein-Barr virus and childhood obesity. We also consider how inequitable health-care access and quality, combined with the younger age of onset and higher comorbidity burdens, might explain racial and ethnic disparities in MS prognosis. Our proposed conceptual model offers a roadmap for generating knowledge and implementing interventions to narrow racial and ethnic disparities in MS susceptibility and outcomes.
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Affiliation(s)
- Annette M Langer-Gould
- Department of Neurology, Los Angeles Medical Center, Southern California Permanente Medical Group, Los Angeles, CA, USA.
- Department of Clinical Science, Kaiser Permanente Bernard J. Tyson School of Medicine, Pasadena, CA, USA.
| | - Tara J Cepon-Robins
- Department of Anthropology, University of Colorado Colorado Springs, Colorado Springs, CO, USA
| | - Jada Benn Torres
- Department of Anthropology, Genetic Anthropology and Biocultural Studies Laboratory, Vanderbilt University, Nashville, TN, USA
- Vanderbilt Genetics Institute, Vanderbilt University Medical Center, Nashville, TN, USA
| | - E Ann Yeh
- Department of Paediatrics Neurology, University of Toronto, Toronto, Ontario, Canada
- Paediatric MS and Neuroinflammatory Disorders Program, The Hospital for Sick Children, Toronto, Ontario, Canada
- Program in Neuroscience and Mental Health, SickKids Research Institute, Toronto, Ontario, Canada
| | - Theresa E Gildner
- Department of Anthropology, Washington University in St. Louis, St. Louis, MO, USA
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Patel A, Wang J, Patel TY, Panchbhavi M, Panchbhavi VK. Assessing the impact of nicotine and non-tobacco nicotine use on postoperative complications following hallux valgus surgery. Foot Ankle Surg 2025:S1268-7731(25)00125-0. [PMID: 40413150 DOI: 10.1016/j.fas.2025.05.008] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/21/2025] [Revised: 05/01/2025] [Accepted: 05/17/2025] [Indexed: 05/27/2025]
Abstract
BACKGROUND Nicotine use, including from non-tobacco sources, is associated with impaired wound healing and increased surgical complications. This study evaluated the impact of nicotine and non-tobacco nicotine use on postoperative outcomes in hallux valgus (HV) surgeries. METHODS Using the TriNetX Global Health Research Network, we analyzed adult patients aged 18 and older undergoing HV correction. Cohorts included nicotine users, non-tobacco nicotine users, and controls, matched using propensity score matching (PSM). Postoperative complications were assessed within 90 days. RESULTS Both nicotine and non-tobacco nicotine cohorts demonstrated increased postoperative complications compared to the control cohort, notably infections, wound disruption, stroke, pneumonia, and renal failure. Also, both nicotine and non-tobacco nicotine users showed elevated healthcare utilization, including emergency department visits and opioid-related disorders. CONCLUSIONS Nicotine and non-tobacco nicotine use significantly increase the risk of postoperative complications following HV surgery, emphasizing the importance of mitigating these risks through further research and preoperative strategies. LEVEL OF EVIDENCE Level III, Retrospective Comparative Study.
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Affiliation(s)
- Apurvakumar Patel
- John Sealy School of Medicine, The University of Texas Medical Branch, 301 University Blvd, Galveston, TX 77555, USA.
| | - Joshua Wang
- John Sealy School of Medicine, The University of Texas Medical Branch, 301 University Blvd, Galveston, TX 77555, USA.
| | - Teerth Y Patel
- John Sealy School of Medicine, The University of Texas Medical Branch, 301 University Blvd, Galveston, TX 77555, USA.
| | - Megna Panchbhavi
- Department of Applied and Computational Mathematics and Statistics, University of Notre Dame, Holy Cross Dr, Notre Dame, IN 46556, USA.
| | - Vinod K Panchbhavi
- Department of Orthopaedic Surgery and Rehabilitation, The University of Texas Medical Branch, 301 University Blvd, Route 0165, Galveston, TX 77555-0165, USA.
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He B, Chen S, Yang X, Olatosi B, Weissman S, Li X, Zhang J. Association between substance use disorders and sustained viral suppression: a longitudinal analysis among people with HIV in South Carolina. AIDS 2025; 39:560-568. [PMID: 39612232 PMCID: PMC11908926 DOI: 10.1097/qad.0000000000004077] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/24/2024] [Accepted: 11/21/2024] [Indexed: 12/01/2024]
Abstract
OBJECTIVES Substance use disorders (SUDs) are a significant public health concern across the United States and may pose a risk to achieving sustained viral suppression (SVS) in people with HIV (PWH). This study aims to examine the association between SUDs and SVS among PWH. DESIGN Using electronic health records from the South Carolina Department of Health, we conducted a retrospective study of adults with HIV who were diagnosed between January 2006 and December 2019. METHODS The impact of SUDs on SVS was assessed using generalized linear mixed model. Potential confounders included age, sex, chronic diseases history, etc. Stepwise selection was performed to decide the confounders included in the final model, and the optimal correlation structure was determined by Akaike information criterion. RESULTS Of the 9412 eligible participants, 7481 (79.48%) had reached SVS status during their follow-up periods. SUDs related to alcohol [adjusted odds ratio (AOR) = 1.70, 95% confidence interval (CI): 1.46-1.98], cannabis (AOR = 1.62, 95% CI: 1.35-1.95), cocaine (AOR = 1.95, 95% CI: 1.60-2.37), opioid (AOR = 1.91, 95% CI: 1.13-3.23), and tobacco (AOR = 1.80, 95% CI: 1.69-1.92) were negatively associated with SVS. Individuals with chronic conditions such as cardiovascular disease (AOR = 0.31, 95% CI: 0.29-0.33), diabetes (AOR = 0.49, 95% CI: 0.41-0.59), and cancer (AOR = 0.47, 95% CI: 0.38-0.58) showed a higher likelihood of maintaining SVS. CONCLUSION This large cohort study of PWH with extended follow-up highlights the negative impact of SUDs on maintaining SVS. Long-term strategies for reducing substance use could support SVS in PWH.
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Affiliation(s)
- Buwei He
- Department of Epidemiology and Biostatistics
| | - Shujie Chen
- Department of Epidemiology and Biostatistics
| | - Xueying Yang
- South Carolina SmartState Center for Healthcare Quality
- Department of Health Promotion, Education and Behavior
| | - Bankole Olatosi
- South Carolina SmartState Center for Healthcare Quality
- Department of Health Services Policy and Management, Arnold School of Public Health
| | - Sharon Weissman
- South Carolina SmartState Center for Healthcare Quality
- Department of Internal Medicine, School of Medicine, University of South Carolina, Columbia, South Carolina, USA
| | - Xiaoming Li
- South Carolina SmartState Center for Healthcare Quality
- Department of Health Promotion, Education and Behavior
| | - Jiajia Zhang
- Department of Epidemiology and Biostatistics
- South Carolina SmartState Center for Healthcare Quality
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Zheng X, Chen Q, Liao Q, Zhang X. Tracking the evolution of serum antibody levels and influencing factors post-SARS-CoV-2 infection among community residents in Fuzhou City. Front Immunol 2025; 16:1533102. [PMID: 40230855 PMCID: PMC11994895 DOI: 10.3389/fimmu.2025.1533102] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/23/2024] [Accepted: 03/12/2025] [Indexed: 04/16/2025] Open
Abstract
Objective To track the level of serum antibodies in Fuzhou residents and analyze the possible influencing factors of serum antibodies, so as to provide a scientific basis for the adjustment of population immunity and prevention and control strategies. Methods Residents in the Fuzhou community who had symptoms of covid-19 infection or who had tested positive for nucleic acid or antigen since December 2022 were selected for the questionnaire survey and their sera were collected to analyze the trend of antibody changes, the antibody level was divided into high antibody group and low antibody group according to the literature data. The possible influencing factors of serum antibody level was analyzed by multivariate logistic regression model. Results A total of 2,521 Fuzhou residents were adopted in the study, including 223 in the high antibody group and 194 in the low antibody group. A univariate analysis showed that, there were significant differences in age (Z=-4.028, P<0.00), occupation (χ2 = 18.591, P=0.005), typical symptoms after the first infection (χ2 = 9.784, P=0.002), history of surgery (χ2 = 29.542, P<0.001), symptoms lasting more than 2 weeks after the first infection (χ2 = 4.887, P=0.027), smoking (χ2 = 18.524, P<0.001) and drinking (χ2 = 19.578, P<0.001) between the high antibody group and the low antibody group. Multivariate regression models show that, age (OR= 1.011, 95%CI: 1.002~1.020, P=0.017), history of surgery (OR=4.956,95%CI: 2.606~9.423, P<0.001),smoking (OR=2.089, 95%CI: 1.002~4.355, P=0.049), drinking (OR=2.214, 95%CI: 1.066~4.600, P=0.033) were the risk factors affecting antibody level. Typical symptoms after the first infection (OR=0.224, 95%CI: 0.086~0.579, P=0.002) and symptoms lasting more than 2 weeks after the first infection (OR=0.432, 95%CI: 0.258~0.723, P=0.001) were protective factors. By observing the trend of antibody changes in 3, 6 and 9 months, we found that the level of IgG antibody showed a decreasing trend. Conclusions The high level of protection was more likely to occur in young adults, people without operation history, people without smoking history, people without drinking history, people with typical symptoms after the first infection and symptoms lasting more than 2 weeks after the first infection. The level of IgG antibody was decreased in general, so it is necessary to strengthen immunization.
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Affiliation(s)
- Xiaoyan Zheng
- The Affiliated Fuzhou Center for Disease Control and Prevention of Fujian Medical University, Fuzhou, China
- The School of Public Health, Fujian Medical University, Fuzhou, China
| | - Qingquan Chen
- The Affiliated Fuzhou Center for Disease Control and Prevention of Fujian Medical University, Fuzhou, China
- The School of Public Health, Fujian Medical University, Fuzhou, China
| | - Qiangbing Liao
- The Affiliated Fuzhou Center for Disease Control and Prevention of Fujian Medical University, Fuzhou, China
- The School of Public Health, Fujian Medical University, Fuzhou, China
| | - Xiaoyang Zhang
- The Affiliated Fuzhou Center for Disease Control and Prevention of Fujian Medical University, Fuzhou, China
- The School of Public Health, Fujian Medical University, Fuzhou, China
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Rodolfi S, Selmi C. Environmental factors and rheumatic diseases. Best Pract Res Clin Rheumatol 2025:102053. [PMID: 40140341 DOI: 10.1016/j.berh.2025.102053] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/10/2025] [Accepted: 02/26/2025] [Indexed: 03/28/2025]
Abstract
The pathogenesis and pathophysiology of rheumatic diseases is complex and relies on the interaction of different factors. The common view is that the pathological autoimmunity develops in genetically predisposed individuals upon exposure to an environmental trigger. This highlights the importance of recognizing and deconstructing the effects of environmental agents in rheumatic diseases. Several factors have been identified in the last decades, with detrimental or protective effects, impacting not only on disease onset, but also on its natural history. Cigarette smoking has been identified as one of the strongest environmental risk factors, being associated with disease development and severity for several rheumatic diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and spondyloarthropathies. Moreover, other airborne pollutants, such as silica, solvents, asbestos and metals are recognized risk factors for rheumatic diseases. The effect of some other agents is however not straightforward, of which a remarkable example is alcohol consumption. Alcohol has been associated with both pro- and anti-inflammatory effects, exerting a variable effect on rheumatic diseases depending on quantity and frequency of consumption, as well as sex and ethnicity. Similarly, ultraviolet light exposure has been associated with a higher risk of SLE but lower risk of RA. The relationship between microbial exposure and autoimmunity is also complex: while some infectious agents increase the risk of rheumatic diseases, it is widely accepted that less exposure to microbial agents, particularly during immune system development, increases the risk of autoimmunity. Furthermore, in recent years the spotlight has switched to the human microbiome, as alterations in organ-specific microbiome composition are anticipated to be early participants in the onset of immune-mediated illnesses. The aim of this review is to highlight the most relevant environmental factors and their role in Rheumatology, with a specific focus on proposed pathophysiological effect and correlation with clinical outcomes.
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Affiliation(s)
- Stefano Rodolfi
- Department of Biomedical Sciences, Humanitas University, Pieve Emanuele, Italy; Department of Rheumatology and Clinical Immunology, IRCCS Humanitas Research Hospital, Rozzano, Italy
| | - Carlo Selmi
- Department of Biomedical Sciences, Humanitas University, Pieve Emanuele, Italy; Department of Rheumatology and Clinical Immunology, IRCCS Humanitas Research Hospital, Rozzano, Italy.
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Johansson E, Olsson T, Alfredsson L, Hedström AK. Impact of lifestyle factors post-infectious mononucleosis on multiple sclerosis risk. Eur J Epidemiol 2025:10.1007/s10654-025-01212-1. [PMID: 40038142 DOI: 10.1007/s10654-025-01212-1] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/03/2024] [Accepted: 02/21/2025] [Indexed: 03/06/2025]
Abstract
BACKGROUND Accumulating evidence suggest that Epstein-Barr virus (EBV) is crucial in the development of multiple sclerosis (MS), with inadequate infection control possibly contributing to disease onset. Past infectious mononucleosis (IM) has been found to interact with smoking, obesity, and sun exposure. We aimed to investigate potential interactions between a history of IM and the following risk factors for MS: passive smoking, alcohol consumption, fish consumption, vitamin D status, adolescent sleep duration and sleep quality. METHODS We analyzed data from a Swedish population-based case-control study (3128 cases and 5986 controls). Subjects were categorized based on IM status and each exposure variable and compared regarding MS risk by calculating odds ratios (OR) with 95% confidence intervals (CI) using logistic regression models. Additive interaction between aspects of IM status and each exposure was assessed by calculating the attributable proportion due to interaction (AP) with 95% CI. RESULTS The OR of developing MS among those who reported a history of IM was 1.86 (95% CI 1.63-2.12), compared with those who had not suffered from IM. We observed synergistic effects between a history of IM and each exposure variable with respect to risk of MS, with significant APs ranging between 0.20 and 0.35. CONCLUSIONS The concept of EBV infection as a crucial factor for MS gains further support from our findings suggesting that MS risk factors synergize with a history of IM in disease development. Targeting modifiable MS risk factors that impede effective immune regulation of the virus holds promise for preventive interventions.
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Affiliation(s)
- Eva Johansson
- Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
| | - Tomas Olsson
- Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
- Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden
| | - Lars Alfredsson
- Centre for Occupational and Environmental Medicine, Region Stockholm, Stockholm, Sweden
- Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
| | - Anna Karin Hedström
- Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
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Al-Alusi NA, Ramirez FD, Chan LN, Ye M, Langan SM, McCulloch C, Abuabara K. Atopic dermatitis and tobacco smoke exposure during childhood and adolescence. THE JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY. GLOBAL 2025; 4:100345. [PMID: 39507926 PMCID: PMC11536054 DOI: 10.1016/j.jacig.2024.100345] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 04/09/2024] [Revised: 07/17/2024] [Accepted: 08/03/2024] [Indexed: 11/08/2024]
Abstract
Background Tobacco smoke may affect atopic dermatitis (AD) because of its known effects on humoral and cellular immunity, but prior studies lack data on disease severity and biomarkers over time. Objective We investigated the association between passive and active tobacco smoke exposure (TSE) during childhood and adolescence and the activity and severity of AD. Methods A birth cohort of 10,521 individuals was followed through adolescence as part of the Avon Longitudinal Study of Parents and Children. We used mixed-effect models to determine the risk of AD (based on repeated assessments) with passive smoke exposure during childhood, active TSE during adolescence, and using a serum biomarker of tobacco exposure (cotinine) at 3 time points. Results After adjusting for confounding factors, there was no evidence of a relationship between passive TSE and concurrent AD activity in childhood (adjusted odds ratio, 0.95; 95% confidence interval, 0.83, 1.07) or of an increased risk between active smoking and AD activity in adolescence (adjusted odds ratio, 0.57; 95% confidence interval, 0.44, 0.75). Secondary analyses demonstrated no dose-response relationship and no increased severity of AD with passive or active TSE. Furthermore, we found no increased risk of AD with a cumulative measure of passive TSE across childhood (adjusted relative risk ratio, 0.98; 95% confidence interval, 0.96, 1.00). Conclusion Neither active nor passive TSE was associated with AD during childhood and adolescence.
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Affiliation(s)
- Noor A. Al-Alusi
- School of Medicine, University of California, San Francisco, Calif
| | | | - Leslie N. Chan
- School of Medicine, University of California, San Francisco, Calif
| | - Morgan Ye
- Department of Dermatology, University of California, San Francisco, Calif
| | - Sinéad M. Langan
- Department of Non-communicable Disease Epidemiology, London School of Hygiene and Tropical Medicine, London, United Kingdom
| | - Chuck McCulloch
- Division of Epidemiology and Biostatistics, University of California, San Francisco, Calif
| | - Katrina Abuabara
- Department of Dermatology, University of California, San Francisco, Calif
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Attauabi M, Madsen GR, Bendtsen F, Burisch J, Seidelin JB. The Role of Environmental Factors Prior to Diagnosis on the Activity and Severity of Inflammatory Bowel Diseases-Results From the Prospective Population-Based Copenhagen Inflammatory Bowel Disease Inception Cohort. United European Gastroenterol J 2025. [PMID: 39878314 DOI: 10.1002/ueg2.12737] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/02/2024] [Revised: 09/30/2024] [Accepted: 10/21/2024] [Indexed: 01/31/2025] Open
Abstract
BACKGROUND The influence of environmental factors on the severity of early inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is unclear. Herein, we aimed to investigate the role of environmental factors in the initial phenotype, activity, and severity of IBD. METHODS Copenhagen IBD Inception Cohort is a prospective population-based cohort of patients with newly diagnosed IBD between May 2021 and May 2023. Data on environmental factors were captured at IBD diagnosis using International Organisation of IBD (IOIBD) and HeartDiet questionnaires. Environmental factors' influence on outcome was analyzed and odds ratios (aOR) were adjusted for age, gender, and disease characteristics (adjusted OR, aOR [95% confidence interval]). RESULTS In total, 208 and 128 patients with incident UC and CD, respectively, were included. Active smoking was associated with increased risk of CD-related hospitalization (aOR = 2.84 [1.03; 7.88]) and stricturing phenotype (aOR = 5.28 [1.76; 15.85]) but lower risk of severe UC course (aOR = 0.28 [0.08; 0.95]). Further, previous smoking was not associated with negative effects in patients with CD in terms of early need for biologics, surgery, or hospitalization. In terms of diets, daily consumption of fruits (aOR = 0.27 [0.07; 0.99]) or vegetables (aOR = 0.27 [0.09; 0.80]) was inversely associated with stricturing CD, whereas whole meal bread was associated with reduced risk of severe CD activity (aOR = 0.40 [0.16; 0.98]). CONCLUSIONS This prospective population-based study highlighted several environmental factors associated with the initial severity and activity of IBD, emphasizing their pivotal role in the initial disease burden and giving guidance to personalized patient counseling.
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Affiliation(s)
- Mohamed Attauabi
- Department of Gastroenterology and Hepatology, Copenhagen University Hospital - Herlev and Gentofte, Herlev, Denmark
- Gastrounit, Medical Section, Copenhagen University Hospital - Amager and Hvidovre, Hvidovre, Denmark
- Copenhagen Center for Inflammatory Bowel Disease in Children, Adolescents, and Adults, Hvidovre Hospital, Hvidovre, Denmark
| | - Gorm Roager Madsen
- Gastrounit, Medical Section, Copenhagen University Hospital - Amager and Hvidovre, Hvidovre, Denmark
- Copenhagen Center for Inflammatory Bowel Disease in Children, Adolescents, and Adults, Hvidovre Hospital, Hvidovre, Denmark
| | - Flemming Bendtsen
- Gastrounit, Medical Section, Copenhagen University Hospital - Amager and Hvidovre, Hvidovre, Denmark
- Copenhagen Center for Inflammatory Bowel Disease in Children, Adolescents, and Adults, Hvidovre Hospital, Hvidovre, Denmark
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
| | - Johan Burisch
- Gastrounit, Medical Section, Copenhagen University Hospital - Amager and Hvidovre, Hvidovre, Denmark
- Copenhagen Center for Inflammatory Bowel Disease in Children, Adolescents, and Adults, Hvidovre Hospital, Hvidovre, Denmark
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
| | - Jakob Benedict Seidelin
- Department of Gastroenterology and Hepatology, Copenhagen University Hospital - Herlev and Gentofte, Herlev, Denmark
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Kayar İ, Goc G, Cetin F, Birge Ö. Impact of Smoking on Cervical Histopathological Changes in High-Risk HPV-Positive Women: A Matched Case-Control Study. MEDICINA (KAUNAS, LITHUANIA) 2025; 61:235. [PMID: 40005352 PMCID: PMC11857344 DOI: 10.3390/medicina61020235] [Citation(s) in RCA: 1] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 12/16/2024] [Revised: 01/13/2025] [Accepted: 01/20/2025] [Indexed: 02/27/2025]
Abstract
Background and Objectives: The aims of this study were to assess the impact of smoking on cervical histopathology in women with high-risk HPV types 16 and 18 (the most common types) utilizing comprehensive clinical data and to conduct a risk analysis based on smoking pack-years. Materials and Methods: Between 2022 and 2024, 1048 high-risk HPV-positive women aged 25 to 65 years were categorized into two groups: smokers and non-smokers. Data acquired from a histopathological examination of samples collected during a colposcopic evaluation of these women were compared individually regarding clinical and demographic factors, specifically age, gravida, parity, and alcohol consumption. Subsequently, the impact of prolonged and excessive smoking on histopathological cellular changes was assessed in women with the same characteristics. A case-control study was performed on 312 smokers and 312 non-smokers following mutual matching. Results: The women were matched one-to-one regarding gravida, parity, and alcohol consumption. Subsequently, they were paired within a ±2-year age range. The mean age of the smoker group was 47.1 ± 8.8, while that of the non-smoker group was 47.2 ± 8.5 (p: 0.904). In all cases of high-risk HPV positivity, the rate of normal cervical cytological results was 14% in women who smoked and 29% in women who did not smoke. The LGSIL, HGSIL, ASC-H, and AGC-NOS rates were elevated in the smoker group, and a statistically significant difference was observed between the two groups in terms of abnormal cervical cytological results (p < 0.001). After a colposcopic biopsy, the smoker group exhibited higher rates of HGSILs, LGSILs, AGC-NOS, and CIS pathological lesions (28% vs. 23%), whereas the non-smoker group exhibited higher rates of chronic cervicitis (23% vs. 16%). However, no statistically significant difference was found between the two groups (p: 0.092). In a comparison of endocervical curettage (ECC) samples, it was observed that the HGSIL, CIS, and AGC-FN rates in the smoker group were almost the same as those in the non-smoker group. However, the LGSIL histopathology results (32% vs. 18%) were higher, and the rate of negativity with no pathology was higher in the non-smoker group (72% vs. 59%). A statistically significant difference in ECC histopathology was noted between the two groups (p < 0.001). An ROC analysis conducted between smoking pack-years and the colposcopic and endocervical curettage biopsy results revealed that the cutoff value for the colposcopic abnormal histopathological results increased, with 40% sensitivity and 76% specificity above 20 pack-years (AUC: 0.592 and p: 0.025). Additionally, the abnormal histopathology rates for endocervical curettage exhibited 81% sensitivity and 32% specificity above 13 pack-years (AUC: 0.586 and p: 0.008). The rate of abnormalities in the colposcopic biopsy results was 2.19 times higher for individuals with over 20 pack-years, and the rate of abnormalities in the ECC results was 2.08 times higher for those with over 13 pack-years; additionally, statistically significant results were obtained (p-values of 0.027 and 0.008, respectively). Conclusions: The most important cause of neoplastic changes in the cervix uteri is high-risk HPV infection, with evidence indicating that prolonged excessive smoking significantly exacerbates the persistence and progression of HPV infection, thereby influencing neoplastic changes in the cervix uteri. It is crucial for women to cease smoking in order to eradicate HPV infection from the body.
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Affiliation(s)
- İlkan Kayar
- Department of Obstetrics and Gynecology, Osmaniye State Hospital, 80000 Osmaniye, Turkey
| | - Goksu Goc
- Department of Obstetrics and Gynecology, American Hospital, 10000 Prishtine, Kosovo;
| | - Ferhat Cetin
- Department of Obstetrics and Gynecology, Private Osmaniye Park Hospital, 80010 Osmaniye, Turkey;
| | - Özer Birge
- Department of Gynecological Oncology, Niger Turkey Friendship Hospital, Niamey G3PR+2JJ, Niger;
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Hua L, Xie M. Heterogeneity and individualized therapy for eosinophilic granulomatosis with polyangiitis. Ther Adv Respir Dis 2025; 19:17534666251318615. [PMID: 39980304 PMCID: PMC11843704 DOI: 10.1177/17534666251318615] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/28/2024] [Accepted: 01/08/2025] [Indexed: 02/22/2025] Open
Abstract
Eosinophilic granulomatosis with polyangiitis (EGPA), as a heterogeneous component of antineutrophil cytoplasmic antibody-associated vasculitis, may be induced by a series of environmental and genetic factors, involved with a variety of immune cells and immune components, and presented with various clinical manifestations, with multiple organs and systems (respiratory, skin, heart, kidney, nerve, etc.) involved. The choice of glucocorticoid (GC) dosage and immunosuppressant in traditional treatment strategies varies greatly from individual to individual and is not universally applicable in all the EGPA phenotype spectrum, especially in relapsing or refractory diseases. With the understanding of the heterogeneity of EGPA, a variety of therapeutic approaches are emerging and improving the traditional treatment model. In this review, we summarized the heterogeneity of EGPA etiology and pathogenesis. Clinical and pathological manifestations of the same organ involved also show significant differences and there are even gender differences. Biological treatments that mainly target type 2 inflammatory pathways are widely used in clinical practice for remission induction and maintenance of EGPA. Targeted biological therapy has shown excellent performance in reducing GC dosage and controlling symptoms and recurrence. However, a large number of high-quality randomized controlled studies are still under research for relapsing or refractory EGPA with special organ involvement. We believe that EGPA has a highly heterogeneous phenotype spectrum, and the treatment patterns targeting key molecules in the pathogenesis are of great value for individual treatment of EGPA.
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Affiliation(s)
- Lijuan Hua
- Department of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China
| | - Min Xie
- Department of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan 430030, Hubei, China
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Michels KB, Dumas O, Varraso R, Camargo CA. Does Asthma Affect the Risk of Developing Breast Cancer? Cancer Med 2025; 14:e70539. [PMID: 39739327 DOI: 10.1002/cam4.70539] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/02/2024] [Revised: 12/10/2024] [Accepted: 12/15/2024] [Indexed: 01/02/2025] Open
Abstract
BACKGROUND The role of the immune system in cancer defense is likely underappreciated. While there has been longstanding interest in the role of atopic diseases in cancer, only a few studies have tested this hypothesis. METHODS We analyzed data from 202,055 women participating in the Nurses' Health Study (NHS) and the Nurses' Health Study II (NHS II) to explore whether asthma is associated with breast cancer. We used Cox proportional hazards models to link physician-diagnosed asthma with subsequent incidence of breast cancer. RESULTS Across the two cohorts, we identified 18,403 cases of physician-diagnosed asthma. During 4,393,760 person-years of follow-up, 11,096 incident cases of breast cancer were diagnosed. In NHS, women with asthma had a covariate-adjusted hazard ratio of 0.92 (95% CI: 0.86-0.99) to develop breast cancer compared to women without asthma; the respective HR in NHS II was 0.93 (0.84-1.03), and 0.92 (0.87-0.98) in the pooled analysis. Among never-smokers, the HR for breast cancer was 0.91 (0.81-1.02) in NHS, 0.81 (0.70-0.93) in NHS II, and 0.86 (0.77-0.97) combined. In two large prospective cohorts of women, participants with asthma had a somewhat lower risk of breast cancer. An active immune system may provide protection from breast cancer. CONCLUSIONS In these longitudinal studies, women with asthma had a somewhat lower risk of breast cancer. This association was most pronounced among never smokers. An active immune system may provide protection from breast cancer.
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Affiliation(s)
- Karin B Michels
- Institute for Prevention and Cancer Epidemiology, Faculty of Medicine and Medical Center, University of Freiburg, Freiburg, Germany
- Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles, California, USA
| | - Orianne Dumas
- Équipe d'Épidémiologie Respiratoire Intégrative, Inserm, CESP, Université Paris-Saclay, UVSQ, Univ. Paris-Sud, Villejuif, France
| | - Raphaelle Varraso
- Équipe d'Épidémiologie Respiratoire Intégrative, Inserm, CESP, Université Paris-Saclay, UVSQ, Univ. Paris-Sud, Villejuif, France
| | - Carlos A Camargo
- Department of Emergency Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA
- Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, USA
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12
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Pangrazzi L, Meryk A. Molecular and Cellular Mechanisms of Immunosenescence: Modulation Through Interventions and Lifestyle Changes. BIOLOGY 2024; 14:17. [PMID: 39857248 PMCID: PMC11760833 DOI: 10.3390/biology14010017] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Received: 11/12/2024] [Revised: 12/17/2024] [Accepted: 12/24/2024] [Indexed: 01/27/2025]
Abstract
Immunosenescence, the age-related decline in immune function, is a complex biological process with profound implications for health and longevity. This phenomenon, characterized by alterations in both innate and adaptive immunity, increases susceptibility to infections, reduces vaccine efficacy, and contributes to the development of age-related diseases. At the cellular level, immunosenescence manifests as decreased production of naive T and B cells, accumulation of memory and senescent cells, thymic involution, and dysregulated cytokine production. Recent advances in molecular biology have shed light on the underlying mechanisms of immunosenescence, including telomere attrition, epigenetic alterations, mitochondrial dysfunction, and changes in key signaling pathways such as NF-κB and mTOR. These molecular changes lead to functional impairments in various immune cell types, altering their proliferative capacity, differentiation, and effector functions. Emerging research suggests that lifestyle factors may modulate the rate and extent of immunosenescence at both cellular and molecular levels. Physical activity, nutrition, stress management, and sleep patterns have been shown to influence immune cell function, inflammatory markers, and oxidative stress in older adults. This review provides a comprehensive analysis of the molecular and cellular mechanisms underlying immunosenescence and explores how lifestyle interventions may impact these processes. We will examine the current understanding of immunosenescence at the genomic, epigenomic, and proteomic levels, and discuss how various lifestyle factors can potentially mitigate or partially reverse aspects of immune aging. By integrating recent findings from immunology, gerontology, and molecular biology, we aim to elucidate the intricate interplay between lifestyle and immune aging at the molecular level, potentially informing future strategies for maintaining immune competence in aging populations.
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Affiliation(s)
- Luca Pangrazzi
- Institute for Biomedical Aging Research, Faculty of Biology, University of Innsbruck, 6020 Innsbruck, Austria;
| | - Andreas Meryk
- Department of Pediatrics, Medical University of Innsbruck, 6020 Innsbruck, Austria
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13
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Kelley J, Buchweitz N, Madden A, Fan H, Hepfer G, Kern M, Townsend DM, Ye T, Yao H, Wu Y. Effect of cigarette smoke exposure and cessation on regional diffusion properties in rat intervertebral discs. JOR Spine 2024; 7:e70015. [PMID: 39544353 PMCID: PMC11561800 DOI: 10.1002/jsp2.70015] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/31/2024] [Revised: 10/21/2024] [Accepted: 10/25/2024] [Indexed: 11/17/2024] Open
Abstract
Background Cigarette smoking is a recognized risk factor for orthopedic disorders, particularly intervertebral disc (IVD) degenerative disease. However, the IVD pathophysiology, especially the spatial-temporal remodeling progression in the context of cigarette smoking, remains unclear. This study aimed to address this knowledge gap through a quantitative assessment of IVD structural composition and diffusion properties using a Sprague-Dawley rat model. Methods Twenty-four rats were divided into control and smoke exposure cohorts, each with two sub-groups of six rats. One smoke exposure sub-group was sacrificed after 2 months of daily cigarette smoke exposure in a custom smoking apparatus, while the other was sacrificed after an additional 5 months of smoke cessation. The control groups were age-matched to the smoke exposure groups. A fluorescent recovery after photobleaching (FRAP) technique was used to determine solute diffusivities and multi-photon excitation (MPE) imaging was performed to characterize structural changes in the annulus fibrosus (AF), nucleus pulposus (NP), and cartilage endplate (CEP). Results A decrease in diffusivity was observed in the CEP and the AF (radial direction only) after 2 months of smoke exposure. MPE imaging showed aberrant CEP calcification and reduced AF radial collagen fiber bundle diameter, suggesting that the IVD exhibits regionally dependent structural remodeling due to smoke exposure. Furthermore, the smoke cessation group showed deteriorating alterations of structure and diffusivities in all three-disc regions, including the NP, indicating that five-month smoke cessation alone didn't reverse the progression of IVD degenerative remodeling during aging. Conclusion This study advances the understanding of IVD pathophysiology in the context of cigarette smoke exposure and cessation, laying the groundwork for potential earlier diagnosis and optimized interventions.
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Affiliation(s)
- Joshua Kelley
- Department of BioengineeringClemson UniversityCharlestonSouth CarolinaUSA
| | - Nathan Buchweitz
- Department of BioengineeringClemson UniversityCharlestonSouth CarolinaUSA
| | - Avery Madden
- Department of BioengineeringClemson UniversityCharlestonSouth CarolinaUSA
| | - Hongming Fan
- Department of BioengineeringClemson UniversityCharlestonSouth CarolinaUSA
| | - Glenn Hepfer
- Department of BioengineeringClemson UniversityCharlestonSouth CarolinaUSA
| | - Michael Kern
- Department of Regenerative Medicine & Cell BiologyMedical University of South CarolinaCharlestonSouth CarolinaUSA
| | - Danyelle M. Townsend
- Department of Drug Discovery and Biomedical SciencesMedical University of South CarolinaCharlestonSouth CarolinaUSA
| | - Tong Ye
- Department of BioengineeringClemson UniversityCharlestonSouth CarolinaUSA
- Department of Regenerative Medicine & Cell BiologyMedical University of South CarolinaCharlestonSouth CarolinaUSA
| | - Hai Yao
- Department of BioengineeringClemson UniversityCharlestonSouth CarolinaUSA
- Department of Oral Health SciencesMedical University of South CarolinaCharlestonSouth CarolinaUSA
| | - Yongren Wu
- Department of BioengineeringClemson UniversityCharlestonSouth CarolinaUSA
- Department of Orthopaedics and Physical MedicineMedical University of South CarolinaCharlestonSouth CarolinaUSA
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14
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Zhan L, Luo S, Wang H, Wang J, Pan X, Lin Y, Jin B, Liang Y, Peng C. Nicotine-Induced Transient Activation of Monocytes Facilitates Immunosuppressive Macrophage Polarization that Restrains T Helper 17 Cell Expansion. Inflammation 2024:10.1007/s10753-024-02191-3. [PMID: 39604662 DOI: 10.1007/s10753-024-02191-3] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/15/2024] [Revised: 11/06/2024] [Accepted: 11/13/2024] [Indexed: 11/29/2024]
Abstract
Macrophages in smoking environment exhibit a distinct immunosuppressive phenotype, but the mechanisms that allow nicotine to "educate" macrophages are incompletely understood. Here, we identified that nicotine transiently activates and subsequently deactivates monocytes, leading to reduced anti-infective capability of macrophages. This deactivation results in a suppression of IL-17-producing cell expansion through decreased IL-1β production. Mechanistically, nicotine induces the expression of IRAK-M in macrophages, which inhibits NF-κB signaling and restrains NLRP3 inflammasome-mediated IL-1β production. Moreover, the induction of IRAK-M by nicotine is mediated through α7 nAChR binding, which activates downstream STAT3 and AKT signaling pathways. Targeting the interaction between nicotine and α7 nAChR can decrease IRAK-M expression and restore LPS-mediated NLRP3 inflammasome-driven IL-1β production. Collectively, these findings elucidate how nicotine modulates macrophage function through complex signaling mechanisms, ultimately impacting their anti-infective responses and inflammatory processes.
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Affiliation(s)
- Lei Zhan
- China Tobacco Guangdong Industrial Co. Ltd, Guangzhou, 510000, China
| | - Siwei Luo
- China Tobacco Guangdong Industrial Co. Ltd, Guangzhou, 510000, China
| | - Han Wang
- China Tobacco Guangdong Industrial Co. Ltd, Guangzhou, 510000, China
| | - Junxia Wang
- China Tobacco Guangdong Industrial Co. Ltd, Guangzhou, 510000, China
| | - Xiaowei Pan
- China Tobacco Guangdong Industrial Co. Ltd, Guangzhou, 510000, China
| | - Yun Lin
- China Tobacco Guangdong Industrial Co. Ltd, Guangzhou, 510000, China
| | - Baofeng Jin
- China Tobacco Guangdong Industrial Co. Ltd, Guangzhou, 510000, China
| | - Yaoxing Liang
- China Tobacco Guangdong Industrial Co. Ltd, Guangzhou, 510000, China
| | - Chen Peng
- China Tobacco Guangdong Industrial Co. Ltd, Guangzhou, 510000, China.
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15
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Plisko O, Zodzika J, Jermakova I, Pcolkina K, Prusakevica A, Liepniece-Karele I, Zarina M, Storozenko J, Rezeberga D. Prediction of high-grade cervical precancerous abnormalities: The role of personal factors, vaginal microflora, sexually transmitted infections, and high-risk human papillomavirus. PLoS One 2024; 19:e0313004. [PMID: 39527583 PMCID: PMC11554082 DOI: 10.1371/journal.pone.0313004] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/07/2024] [Accepted: 10/16/2024] [Indexed: 11/16/2024] Open
Abstract
High-risk human papillomavirus infection (HR-HPV) is necessary but not the only factor needed to develop cervical cancer. It is essential to estimate cervical cancer development risk in the population of high-risk HPV-positive women and to avoid unnecessary examinations and treatment in low-risk individuals. The study aimed to identify associations between different personal factors, vaginal microflora, sexually transmitted, high-risk HPV infection, and various degrees of cervical precancerous lesions. A study was performed in 2016-2020. The study group consisted of 112 patients with abnormal cervical cytology results referred for colposcopic examination. 120 women who came for a routine gynecological check-up were included in the control group. Material from the cervix and upper vaginal fornix was taken for pH measurement, wet mount microscopy, testing the six most common high-risk HPV DNA types (16/18, 31, 33, 45, 58), HPV E6/E7 mRNA, and 7 genital infections-C. trachomatis, N. gonorrhea, T. vaginalis, M. hominis, M. genitalium, U. urealyticum, U. parvum. Results showed that women with all grades of cervical intraepithelial neoplasia (CIN) more often were smokers, had increased vaginal pH levels, and had positive HR-HPV DNA and HR HPV E6/E7 mRNA expression. Abnormal vaginal microflora, especially types associated with aerobic vaginitis, and M. hominis were significantly more often found in women with CIN2+. The presence of C.trachomatis, U. parvum, and U.urealyticum did not differ between the groups. The most important factors independently associated with CIN2+ were positive high-risk HPV E6/E7 mRNA expression (OR 59.4, 95% CI 14.84-237.51), and positive high-risk HPV DNA (OR 3.9, 95% CI 1.16-13.23). Higher education level was associated with reduced risk of CIN2+ (OR 0.2, 95% CI 0.07-0.71). In conclusion, this study reports HR-HPV DNA of the most common six types and E6/E7 mRNA positivity as the most significant factors associated with CIN2+ lesions and higher education related to lower risk of high-grade cervical lesions.
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Affiliation(s)
- Olga Plisko
- Department of Obstetrics and Gynecology, Riga Stradins University, Riga, Latvia
- Gynecological Clinic, Riga East Clinical University Hospital, Riga, Latvia
| | - Jana Zodzika
- Department of Obstetrics and Gynecology, Riga Stradins University, Riga, Latvia
- Gynecological Clinic, Riga East Clinical University Hospital, Riga, Latvia
| | - Irina Jermakova
- Department of Obstetrics and Gynecology, Riga Stradins University, Riga, Latvia
- Gynecological Clinic, Riga East Clinical University Hospital, Riga, Latvia
| | - Kristine Pcolkina
- Gynecological Clinic, Riga East Clinical University Hospital, Riga, Latvia
| | | | - Inta Liepniece-Karele
- Department of Pathology, Riga Stradins University, Riga, Latvia
- Pathology Center, Riga East Clinical University Hospital, Riga, Latvia
| | - Marta Zarina
- Department of Infectology, Riga Stradins University, Riga, Latvia
- Central Laboratory, Riga, Latvia
| | - Jelena Storozenko
- Department of Infectology, Riga Stradins University, Riga, Latvia
- Central Laboratory, Riga, Latvia
| | - Dace Rezeberga
- Department of Obstetrics and Gynecology, Riga Stradins University, Riga, Latvia
- Gynecological Clinic, Riga East Clinical University Hospital, Riga, Latvia
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16
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Valeriani F, Protano C, Pozzoli A, Vitale K, Liguori F, Liguori G, Gallè F. Does Tobacco Smoking Affect Vaccine-Induced Immune Response? A Systematic Review and Meta-Analysis. Vaccines (Basel) 2024; 12:1260. [PMID: 39591163 PMCID: PMC11599009 DOI: 10.3390/vaccines12111260] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/08/2024] [Revised: 11/02/2024] [Accepted: 11/05/2024] [Indexed: 11/28/2024] Open
Abstract
Background. Causing approximately 8 million deaths each year, tobacco smoking represents a significant public health concern. Evidence shows that smoking significantly impairs antibody production and immune cell activity following vaccination. Objectives. This review aims to provide a comprehensive overview of the literature regarding how smoking reduces the effectiveness of active immunization by affecting vaccine-induced immune response. Methods. This study was performed according to the PRISMA guidelines, and the protocol was registered on the PROSPERO platform (ID: CRD42024582638). PubMed, Scopus and Web of Science were consulted as bibliographic and citation databases. Studies published in Italian and English and that aimed to investigate the effects of exposure to active and passive tobacco smoking on vaccine-induced immune response were included. Results. Thirty-four studies were selected. Overall, a decrease in antibody levels and avidity and in immune cell production were observed in individuals exposed to smoke. The meta-analysis showed a weighted mean difference between smokers and non-smokers equal to 0.65 (95% CI: 0.10-1.19, p = 0.02) for vaccinations against COVID-19, influenza, pneumococcus, HBV, HPV, tetanus, pertussis, polio, haemophilus influenzae type b, measles-mumps-rubella, and recurrent urinary tract infections. Conclusions. Smoking cessation campaigns should be considered in order to increase the effectiveness of vaccination programs. Furthermore, the opportunity to adopt different vaccine dosing schemes for smokers and non-smokers, especially in acute epidemics, should be considered.
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Affiliation(s)
- Federica Valeriani
- Department of Movement, Human, and Health Sciences, University of Rome Foro Italico, 00135 Rome, Italy;
| | - Carmela Protano
- Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00161 Rome, Italy; (C.P.); (A.P.); (K.V.)
| | - Angela Pozzoli
- Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00161 Rome, Italy; (C.P.); (A.P.); (K.V.)
| | - Katia Vitale
- Department of Public Health and Infectious Diseases, Sapienza University of Rome, 00161 Rome, Italy; (C.P.); (A.P.); (K.V.)
| | - Fabrizio Liguori
- Department of Economics and Legal Studies, University of Naples “Parthenope”, Via Generale Parisi 13, 80132 Naples, Italy;
| | - Giorgio Liguori
- Department of Medical, Movement and Wellbeing Sciences, University of Naples “Parthenope”, 80133 Naples, Italy;
| | - Francesca Gallè
- Department of Medical, Movement and Wellbeing Sciences, University of Naples “Parthenope”, 80133 Naples, Italy;
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17
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Tan Q, Xu X, Zhou H, Jia J, Jia Y, Tu H, Zhou D, Wu X. A multi-ancestry cerebral cortex transcriptome-wide association study identifies genes associated with smoking behaviors. Mol Psychiatry 2024; 29:3580-3589. [PMID: 38816585 DOI: 10.1038/s41380-024-02605-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/28/2023] [Revised: 04/30/2024] [Accepted: 05/09/2024] [Indexed: 06/01/2024]
Abstract
Transcriptome-wide association studies (TWAS) have provided valuable insight in identifying genes that may impact cigarette smoking. Most of previous studies, however, mainly focused on European ancestry. Limited TWAS studies have been conducted across multiple ancestries to explore genes that may impact smoking behaviors. In this study, we used cis-eQTL data of cerebral cortex from multiple ancestries in MetaBrain, including European, East Asian, and African samples, as reference panels to perform multi-ancestry TWAS analyses on ancestry-matched GWASs of four smoking behaviors including smoking initiation, smoking cessation, age of smoking initiation, and number of cigarettes per day in GWAS & Sequencing Consortium of Alcohol and Nicotine use (GSCAN). Multiple-ancestry fine-mapping approach was conducted to identify credible gene sets associated with these four traits. Enrichment and module network analyses were further performed to explore the potential roles of these identified gene sets. A total of 719 unique genes were identified to be associated with at least one of the four smoking traits across ancestries. Among those, 249 genes were further prioritized as putative causal genes in multiple ancestry-based fine-mapping approach. Several well-known smoking-related genes, including PSMA4, IREB2, and CHRNA3, showed high confidence across ancestries. Some novel genes, e.g., TSPAN3 and ANK2, were also identified in the credible sets. The enrichment analysis identified a series of critical pathways related to smoking such as synaptic transmission and glutamate receptor activity. Leveraging the power of the latest multi-ancestry GWAS and eQTL data sources, this study revealed hundreds of genes and relevant biological processes related to smoking behaviors. These findings provide new insights for future functional studies on smoking behaviors.
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Affiliation(s)
- Qilong Tan
- Department of Big Data in Health Science School of Public Health, Center of Clinical Big Data and Analytics of The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310058, China
- The Key Laboratory of Intelligent Preventive Medicine of Zhejiang Province, Hangzhou, 310058, China
| | - Xiaohang Xu
- Department of Big Data in Health Science School of Public Health, Center of Clinical Big Data and Analytics of The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310058, China
- The Key Laboratory of Intelligent Preventive Medicine of Zhejiang Province, Hangzhou, 310058, China
| | - Hanyi Zhou
- Department of Big Data in Health Science School of Public Health, Center of Clinical Big Data and Analytics of The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310058, China
- The Key Laboratory of Intelligent Preventive Medicine of Zhejiang Province, Hangzhou, 310058, China
| | - Junlin Jia
- Department of Big Data in Health Science School of Public Health, Center of Clinical Big Data and Analytics of The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310058, China
- The Key Laboratory of Intelligent Preventive Medicine of Zhejiang Province, Hangzhou, 310058, China
| | - Yubing Jia
- Department of Big Data in Health Science School of Public Health, Center of Clinical Big Data and Analytics of The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310058, China
- The Key Laboratory of Intelligent Preventive Medicine of Zhejiang Province, Hangzhou, 310058, China
| | - Huakang Tu
- Department of Big Data in Health Science School of Public Health, Center of Clinical Big Data and Analytics of The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310058, China
- The Key Laboratory of Intelligent Preventive Medicine of Zhejiang Province, Hangzhou, 310058, China
- National Institute for Data Science in Health and Medicine, Zhejiang University, Hangzhou, Zhejiang, China
| | - Dan Zhou
- Department of Big Data in Health Science School of Public Health, Center of Clinical Big Data and Analytics of The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310058, China
- The Key Laboratory of Intelligent Preventive Medicine of Zhejiang Province, Hangzhou, 310058, China
- Cancer Center, Zhejiang University, Hangzhou, 310058, China
| | - Xifeng Wu
- Department of Big Data in Health Science School of Public Health, Center of Clinical Big Data and Analytics of The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310058, China.
- The Key Laboratory of Intelligent Preventive Medicine of Zhejiang Province, Hangzhou, 310058, China.
- School of Medicine and Health Science, George Washington University, Washington, DC, USA.
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Villatte G, Haverlan A, Le Baron M, Mulliez A, Boisgard S, Descamps S, Erivan R. Epidemiology of complications after non-compulsory planned hardware-removal after limbs fracture. Orthop Traumatol Surg Res 2024:104028. [PMID: 39433175 DOI: 10.1016/j.otsr.2024.104028] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/13/2024] [Revised: 08/27/2024] [Accepted: 09/18/2024] [Indexed: 10/23/2024]
Abstract
INTRODUCTION Removal of hardware (HR) following a fracture is a frequent question from patients. The incidence of this kind of intervention remains very variable depending on the healthcare systems and its interest is debated in view of the benefits and associated risks that remain poorly defined. Mandatory preoperative information cannot be given optimally in this context. OBJECTIVE To determine the rate of complications (major and minor) after non-compulsory planned hardware-removal following a limb fracture. HYPOTHESIS The rate of major complications was greater than 1%. METHODS A 10-year retrospective single-center study included 1990 patients who had undergone routine HR. Analysis of medical records, with a minimum of one year of follow-up, allowed us to collect: patient data, the type and anatomical location of the osteosynthesis material, as well as the occurrence of a postoperative complication, categorized as a major complication (resulting in either a new surgical procedure, re-hospitalization, or lasting functional impairment) or a minor complication. RESULTS Overall, 4.1% (79/1990) of patients experienced postoperative complications, including 1.56% (31/1990) major complications and 21 surgical revisions (1.06%). The time to onset of complications was 9.1 +/- 8.4 days. The most common complications were deep infections and impaired skin healing with superficial infection (55/79, 69.6%). Locations "around the knee" and "around the ankle" were at higher risk of complications (p < 0.01). Smoking was identified as a significant risk factor for complications, particularly deep infection (p = 0.004, OR = 8.7 [1.98; 38.11]). DISCUSSION Non-mandatory routine RH has a significant complication rate even in a healthy population. Preoperative information of the patient and the assessment of the benefit/risk balance are essential in this indication. This study also raises the question of mandatory smoking cessation preoperatively. LEVEL OF EVIDENCE IV; retrospective study.
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Affiliation(s)
- Guillaume Villatte
- Université Clermont Auvergne, CHU Clermont-Ferrand, CNRS, SIGMA Clermont, ICCF, F-63000 Clermont-Ferrand, France; Service d'orthopédie-traumatologie, CHU Montpied Clermont-Ferrand, 63000 Clermont-Ferrand, France.
| | - Arthur Haverlan
- Service d'orthopédie-traumatologie, CHU Montpied Clermont-Ferrand, 63000 Clermont-Ferrand, France
| | - Marie Le Baron
- Service de chirurgie orthopédique, hôpital Nord, pôle locomoteur, Institut du mouvement et de l'appareil locomoteur, Assistance publique-Hôpitaux de Marseille, Marseille, France
| | - Aurélien Mulliez
- Department of Clinical Research and Innovation DRCI, CHU Montpied Clermont-Ferrand, 63000 Clermont-Ferrand, France
| | - Stéphane Boisgard
- Université Clermont Auvergne, CHU Clermont-Ferrand, CNRS, SIGMA Clermont, ICCF, F-63000 Clermont-Ferrand, France; Service d'orthopédie-traumatologie, CHU Montpied Clermont-Ferrand, 63000 Clermont-Ferrand, France
| | - Stéphane Descamps
- Université Clermont Auvergne, CHU Clermont-Ferrand, CNRS, SIGMA Clermont, ICCF, F-63000 Clermont-Ferrand, France; Service d'orthopédie-traumatologie, CHU Montpied Clermont-Ferrand, 63000 Clermont-Ferrand, France
| | - Roger Erivan
- Université Clermont Auvergne, CHU Clermont-Ferrand, CNRS, SIGMA Clermont, ICCF, F-63000 Clermont-Ferrand, France; Service d'orthopédie-traumatologie, CHU Montpied Clermont-Ferrand, 63000 Clermont-Ferrand, France
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19
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Al-Shalabi E, Sunoqrot S, Al-Zuhd T, Alshehada RS, Ibrahim AIM, Hammad AM. Exploring the Antioxidant and Anti-Inflammatory Effects of Rhoifolin Isolated from Teucrium Polium on Rats' Lungs Exposed to Tobacco Smoke. Chem Biodivers 2024; 21:e202400958. [PMID: 39001681 DOI: 10.1002/cbdv.202400958] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/17/2024] [Accepted: 07/12/2024] [Indexed: 10/16/2024]
Abstract
Cigarette smoking exacerbates respiratory diseases, while plant-derived polyphenols offer antioxidant and anti-inflammatory benefits. This study exploresd the effects of Rhoifolin (ROF), a polyphenol from Jordanian Teucrium polium, on lung health in rats exposed to tobacco smoke. Male rats were divided into two groups: one exposed to cigarette smoke (CS), and the other to ROF treatment alongside smoke exposure (CS/ROF). ROF was administered orally for 21 days before smoke exposure. Results showed smoke-induced lung inflammation and oxidative stress, mitigated by ROF treatment. Histological examination revealed smoke-related morphological changes in lung tissue. ROF treatment reduced oxidative stress and inflammation, as evidenced by decreased proinflammatory cytokines. In silico docking demonstrated ROF's potential as an inhibitor of proinflammatory cytokines. This study demonstrates the therapeutic potential of ROF and similar polyphenols in mitigating the harmful effects of cigarette smoke on lung health.
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Affiliation(s)
- Eveen Al-Shalabi
- Department of Pharmacy, Faculty of Pharmacy, Al-Zaytoonah University of Jordan, Amman, 11733, Jordan
| | - Suhair Sunoqrot
- Department of Pharmacy, Faculty of Pharmacy, Al-Zaytoonah University of Jordan, Amman, 11733, Jordan
| | - Thanaa Al-Zuhd
- Department of Pharmacy, Faculty of Pharmacy, Al-Zaytoonah University of Jordan, Amman, 11733, Jordan
| | - Rahaf S Alshehada
- Department of Pharmacy, Faculty of Pharmacy, Al-Zaytoonah University of Jordan, Amman, 11733, Jordan
| | - Ali I M Ibrahim
- Department of Pharmacy, Faculty of Pharmacy, Al-Zaytoonah University of Jordan, Amman, 11733, Jordan
| | - Alaa M Hammad
- Department of Pharmacy, Faculty of Pharmacy, Al-Zaytoonah University of Jordan, Amman, 11733, Jordan
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Vestergaard C. The complex relationship between maternal smoking and atopic dermatitis in children. J Eur Acad Dermatol Venereol 2024; 38:1840-1841. [PMID: 39319940 DOI: 10.1111/jdv.20260] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/18/2024] [Accepted: 07/18/2024] [Indexed: 09/26/2024]
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Zhao B, Xue J, Zhang H. Causal effects of smoking, alcohol consumption, and coffee intake on hepatobiliary and pancreatic diseases: A Mendelian randomization study. Clin Res Hepatol Gastroenterol 2024; 48:102450. [PMID: 39168247 DOI: 10.1016/j.clinre.2024.102450] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/24/2024] [Revised: 08/14/2024] [Accepted: 08/18/2024] [Indexed: 08/23/2024]
Abstract
BACKGROUND Hepatobiliary and pancreatic diseases, such as cirrhosis, hepatocellular carcinoma, cholelithiasis, and pancreatitis, are major global health challenges. Lifestyle factors like smoking, alcohol consumption, and coffee intake are commonly studied for their health impacts. However, observational studies often face issues with confounding factors and reverse causality, making it difficult to establish causal relationships. METHODS This research uses Mendelian randomization (MR) to investigate the causal effects of smoking, alcohol use, and coffee intake on 10 hepatobiliary and pancreatic diseases. Genetic data from the Sequencing Consortium of Alcohol and Nicotine Use (GSCAN) and self-reported GWAS were used to derive instrumental variables (IVs). The outcomes were obtained from the FinnGen and UK Biobank cohorts. Univariable and multivariable MR analyses were conducted to assess the associations. RESULTS Genetic predisposition to tobacco use was associated with increased risks of acute pancreatitis, alcoholic hepatitis, chronic pancreatitis, cirrhosis, gallstones, liver cancer, and pancreatic cancer. Alcohol consumption was linked to acute pancreatitis, chronic pancreatitis, alcoholic liver disease, hepatic cancer, and cholangitis. Coffee intake showed minimal associations, with a slight protective effect against non-alcoholic steatohepatitis. CONCLUSIONS This study confirms the harmful effects of inhaling tobacco and consuming alcohol on hepatobiliary and pancreatic diseases. It highlights the need for public health strategies to reduce tobacco use and heavy alcohol consumption. Coffee intake showed minimal effects, suggesting further research is needed to understand its relationship with hepatobiliary health.
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Affiliation(s)
- Bingbing Zhao
- Yan'an People's Hospital, Shanxi Province, 716000, PR China
| | - Jiajing Xue
- Graduate Division of Xi'an Medical University, Shanxi Province, 710021, PR China
| | - Huaqin Zhang
- Yan'an People's Hospital, Shanxi Province, 716000, PR China.
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Falara E, Metallinou D, Nanou C, Vlachou M, Diamanti A. Perinatal Exposure to Tobacco Smoke and Its Association with the Maternal and Offspring Microbiome: A Systematic Review. Healthcare (Basel) 2024; 12:1874. [PMID: 39337215 PMCID: PMC11431162 DOI: 10.3390/healthcare12181874] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/30/2024] [Revised: 09/11/2024] [Accepted: 09/12/2024] [Indexed: 09/30/2024] Open
Abstract
BACKGROUND The human microbiome, comprising trillions of microorganisms, significantly influences human health and disease. During critical periods like the perinatal phase, the microbiome undergoes significant changes, impacting lifelong health. Tobacco smoke, a known environmental pollutant, has adverse effects on health, particularly during pregnancy. Despite this, its association with the perinatal microbiome remains understudied. METHODS We conducted a systematic review to integrate findings on perinatal tobacco smoke exposure and its association with the maternal and neonatal microbiomes. We conducted a comprehensive literature search in the PubMed, Scopus, and Web of Science databases from January 2000 to February 2024. We selected studies that met predefined inclusion criteria and performed data extraction. RESULTS The review included eight studies that revealed diverse associations of perinatal tobacco exposure with the maternal and neonatal microbiome. Active smoking during pregnancy was linked to alterations in microbiome composition and diversity in children. Maternal smoking correlated with increased Firmicutes abundance and decreased Akkermansia muciniphila abundance in offspring. Additionally, exposure to thirdhand smoke in neonatal intensive care units was related to infant microbiome diversity. Infants exposed to tobacco smoke showed various microbial changes, suggesting potential implications for childhood health outcomes, including obesity risk. CONCLUSIONS Perinatal exposure to tobacco smoke exerts significant influence on the maternal and neonatal microbiomes, with potential implications for long-term health outcomes. Addressing socioeconomic and psychological barriers to smoking cessation, implementing stricter smoking regulations, and promoting public health campaigns are essential steps towards reducing tobacco-related harm during the perinatal period. Further longitudinal studies and standardized assessment methods are needed to validate these findings and guide the development of effective preventive measures.
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Affiliation(s)
| | | | | | - Maria Vlachou
- Department of Midwifery, Faculty of Health and Caring Sciences, University of West Attica, 12243 Egaleo, Greece; (E.F.); (D.M.); (C.N.); (A.D.)
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González Zarzar T, Palmiero NE, Kim D, Shen L, Hall MA. Differential effects of environmental exposures on clinically relevant endophenotypes between sexes. Sci Rep 2024; 14:21453. [PMID: 39271740 PMCID: PMC11399237 DOI: 10.1038/s41598-024-72180-x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/23/2024] [Accepted: 09/04/2024] [Indexed: 09/15/2024] Open
Abstract
Sex and gender differences play a crucial role in health and disease outcomes. This study used data from the National Health and Nutrition Examination Survey to explore how environmental exposures affect health-related traits differently in males and females. We utilized a sex-stratified phenomic environment-wide association study (PheEWAS), which allowed the identification of associations across a wide range of phenotypes and environmental exposures. We examined associations between 272 environmental exposures, including smoking-related exposures such as cotinine levels and smoking habits, and 58 clinically relevant blood phenotypes, such as serum albumin and homocysteine levels. Our analysis identified 119 sex-specific associations. For example, smoking-related exposures had a stronger impact on increasing homocysteine, hemoglobin, and hematocrit levels in females while reducing serum albumin and bilirubin levels and increasing c-reactive protein levels more significantly in males. These findings suggest mechanisms by which smoking exposure may pose higher cardiovascular risks and greater induced hypoxia for women, and greater inflammatory and immune responses in men. The results highlight the importance of considering sex differences in biomedical research. Understanding these differences can help develop more personalized and effective health interventions and improve clinical outcomes for both men and women.
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Affiliation(s)
- Tomás González Zarzar
- School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
- Institute for Biological and Medical Engineering, Pontificia Universidad Católica de Chile, Santiago, Chile.
| | - Nicole E Palmiero
- Institute for Biomedical Informatics, Department of Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA
| | - Dokyoon Kim
- Department of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA
| | - Li Shen
- Department of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA
| | - Molly A Hall
- Institute for Biomedical Informatics, Department of Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA
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Gao KX, Yang YH, Liang Q, Mei LY, Liang YB, Wang MJ, Chen XM, Huang QC, Wen ZH, Huang RY. Targeting Therapeutic Windows for Rheumatoid Arthritis Prevention. Chin J Integr Med 2024; 30:842-851. [PMID: 38753276 DOI: 10.1007/s11655-024-3760-2] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 03/15/2024] [Indexed: 08/25/2024]
Abstract
Rheumatoid arthritis (RA) is a worldwide public health problem. Interventions to delay or prevent the onset of RA have attracted much attention in recent years, and researchers are now exploring various prevention strategies. At present, there is still no unified consensus for RA prevention, but targeting therapeutic windows and implementing interventions for at-risk individuals are extremely important. Due to the limited number of clinical trials on pharmacologic interventions, further studies are needed to explore and establish optimal intervention regimens and effective measures to prevent progression to RA. In this review, we introduce the RA disease process and risk factors, and present research on the use of both Western and Chinese medicine from clinical perspectives regarding RA prevention. Furthermore, we describe several complete and ongoing clinical studies on the use of Chinese herbal formulae for the prevention of RA.
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Affiliation(s)
- Kai-Xin Gao
- Section of Rheumatology and Immunology Research, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China
| | - Yi-Hong Yang
- The Second Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China
| | - Qi Liang
- The Second Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China
| | - Li-Yan Mei
- Section of Rheumatology and Immunology Research, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China
| | - You-Bang Liang
- The Second Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China
| | - Mao-Jie Wang
- Section of Rheumatology and Immunology Research, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China
- State Key Laboratory of Dampness Syndrome of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China
- Guangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China
- Guangdong Provincial Key Laboratory of Clinical Research on Traditional Chinese Medicine Syndrome, Guangzhou, 510120, China
| | - Xiu-Min Chen
- Section of Rheumatology and Immunology Research, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China
- State Key Laboratory of Dampness Syndrome of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China
- Guangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China
- Guangdong Provincial Key Laboratory of Clinical Research on Traditional Chinese Medicine Syndrome, Guangzhou, 510120, China
| | - Qing-Chun Huang
- Section of Rheumatology and Immunology Research, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China
- State Key Laboratory of Dampness Syndrome of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China
- Guangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China
- Guangdong Provincial Key Laboratory of Chinese Medicine for Prevention and Treatment of Refractory Chronic Diseases, Guangzhou, 510120, China
| | - Ze-Huai Wen
- The Key Unit of Methodology of Clinical Research, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China
| | - Run-Yue Huang
- Section of Rheumatology and Immunology Research, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
- State Key Laboratory of Dampness Syndrome of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
- Guangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
- Guangdong Provincial Key Laboratory of Clinical Research on Traditional Chinese Medicine Syndrome, Guangzhou, 510120, China.
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Alemohammad SY, Khalaji A, Osibogun O, Jebai R, Li W, Ijaz A, Gehris M, Abbasabad GD, Ward KD, Bursac Z, Taleb ZB, Kalan ME. Associations between ENDS and cigarette use, and compromised immunity in US adults: Findings from the 2021-2022 NHIS. J Addict Dis 2024:1-10. [PMID: 39066465 PMCID: PMC11762369 DOI: 10.1080/10550887.2024.2380116] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 07/28/2024]
Abstract
BACKGROUND Tobacco use presents increased risks for individuals with weakened immune systems (WIS). We investigated the association between cigarette and electronic nicotine delivery systems (ENDS or e-cigarettes) use and WIS in US adults using data from the 2021-2022 National Health Interview Survey. METHODS Data from 57,133 adults were analyzed, focusing on WIS prevalence due to health conditions, prescriptions, or both. Cigarette and ENDS use were categorized as never, former, or current. Weighted multivariable regression models adjusted for demographics and other health conditions to assess associations between tobacco use and WIS. RESULTS Among US adults, 4.3% had prescription-related WIS, 4.6% had health condition-related WIS, and 7% had WIS due to either reason. Adjusted results from multivariable regression models indicated that adults with WIS due to health conditions were more likely to be current (AOR = 1.21, 95%CI: 1.05-1.40) and former (AOR = 1.25, 95%CI: 1.11-1.39) cigarette smokers compared to counterparts without WIS. Adults with WIS due to prescriptions were more likely to be former cigarette smokers (AOR = 1.19, 95%CI: 1.06-1.34). Those with WIS for any reason were more likely to be current (AOR = 1.19, 95%CI: 1.05-1.35) and former (AOR = 1.24, 95%CI: 1.13-1.36) cigarette smokers. Adults with WIS due to health conditions (AOR = 1.23, 95%CI: 1.06-1.41) or any reasons (AOR = 1.19, 95%CI:1.05-1.34) were more likely to be former ENDS users compared to those without WIS. CONCLUSIONS In this nationally representative study, we found a notable link between cigarette and ENDS use with WIS, particularly among those with health condition-related or prescription-related WIS, underscoring the importance of addressing tobacco use in this vulnerable population.
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Affiliation(s)
- Seyedeh Yasaman Alemohammad
- Department of Epidemiology, Robert Stempel College of Public Health, Florida International University, Miami, FL, USA
| | | | - Olatokunbo Osibogun
- Department of Epidemiology, Robert Stempel College of Public Health, Florida International University, Miami, FL, USA
| | - Rime Jebai
- Department of Health Law, Policy & Management, Boston University, Boston, USA
| | - Wei Li
- Department of Psychiatry, Yale School of Medicine, New Haven, CT, USA
| | - Ateeqa Ijaz
- School of Health Professions, Eastern Virginia Medical School, Norfolk, VA, USA
| | - Miranda Gehris
- School of Health Professions, Eastern Virginia Medical School, Norfolk, VA, USA
| | - Ghader Dargahi Abbasabad
- Department of Social and Behavioral Science, Virginia Commonwealth University, Richmond, VA, USA
| | - Kenneth D Ward
- College of Population Health, University of New Mexico, Albuquerque, NM, USA
| | - Zoran Bursac
- Department of Biostatistics, Robert Stempel College of Public Health, Florida International University, Miami, FL, USA
| | - Ziyad Ben Taleb
- Department of Kinesiology, College of Nursing and Health Innovation, University of Texas at Arlington, Arlington, TX, USA
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Djouina M, Ollivier A, Waxin C, Kervoaze G, Pichavant M, Caboche S, Achour D, Grare C, Beury D, Hot D, Anthérieu S, Lo-Guidice JM, Dubuquoy L, Launay D, Vignal C, Gosset P, Body-Malapel M. Chronic Exposure to Both Electronic and Conventional Cigarettes Alters Ileum and Colon Turnover, Immune Function, and Barrier Integrity in Mice. J Xenobiot 2024; 14:950-969. [PMID: 39051349 PMCID: PMC11270428 DOI: 10.3390/jox14030053] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/30/2024] [Revised: 07/11/2024] [Accepted: 07/13/2024] [Indexed: 07/27/2024] Open
Abstract
Although the effects of cigarette smoke (CS) on the development of several intestinal diseases is well documented, the impact of e-cigarette aerosol (e-cig) on digestive health is largely unknown. To compare the effects of e-cig and CS on mouse ileum and colon, animals were chronically exposed for 6 months by nose-only inhalation to e-cig at 18 or 30 W power, or to 3R4F CS. Results showed that e-cig exposure decreased colon cell proliferation. Several other proliferative defects were observed in response to both e-cig and CS exposure, including up- and down-regulation of cyclin D1 protein levels in the ileum and colon, respectively. E-cig and CS exposure reduced myeloperoxidase activity in the ileum. In the colon, both exposures disrupted gene expression of cytokines and T cell transcription factors. For tight junction genes, ZO-1- and occludin-protein expression levels were reduced in the ileum and colon, respectively, by e-cig and CS exposure. The 16S sequencing of microbiota showed specific mild dysbiosis, according to the type of exposure. Overall, e-cig exposure led to altered proliferation, inflammation, and barrier function in both the ileum and colon, and therefore may be a gut hazard on par with conventional CS.
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Affiliation(s)
- Madjid Djouina
- Univ. Lille, Inserm, CHU Lille, U1286-INFINITE—Institute for Translational Research in Inflammation, F-59000 Lille, France; (M.D.); (C.W.); (L.D.); (D.L.); (C.V.)
| | - Anaïs Ollivier
- Univ. Lille, CNRS, INSERM, Institut Pasteur de Lille, CHU Lille, Center for Infection and Immunity of Lille (CIIL), UMR9017-U1019, F-59000 Lille, France; (A.O.); (G.K.); (M.P.); (P.G.)
| | - Christophe Waxin
- Univ. Lille, Inserm, CHU Lille, U1286-INFINITE—Institute for Translational Research in Inflammation, F-59000 Lille, France; (M.D.); (C.W.); (L.D.); (D.L.); (C.V.)
| | - Gwenola Kervoaze
- Univ. Lille, CNRS, INSERM, Institut Pasteur de Lille, CHU Lille, Center for Infection and Immunity of Lille (CIIL), UMR9017-U1019, F-59000 Lille, France; (A.O.); (G.K.); (M.P.); (P.G.)
| | - Muriel Pichavant
- Univ. Lille, CNRS, INSERM, Institut Pasteur de Lille, CHU Lille, Center for Infection and Immunity of Lille (CIIL), UMR9017-U1019, F-59000 Lille, France; (A.O.); (G.K.); (M.P.); (P.G.)
| | - Ségolène Caboche
- Univ. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, US41-UAR 2014-PLBS, F-59000 Lille, France; (S.C.); (D.B.); (D.H.)
| | - Djamal Achour
- Univ. Lille, CHU Lille, Institut Pasteur de Lille, ULR 4483-IMPECS—IMPact de l’Environnement Chimique sur la Santé, F-59000 Lille, France; (D.A.); (C.G.); (S.A.); (J.-M.L.-G.)
| | - Céline Grare
- Univ. Lille, CHU Lille, Institut Pasteur de Lille, ULR 4483-IMPECS—IMPact de l’Environnement Chimique sur la Santé, F-59000 Lille, France; (D.A.); (C.G.); (S.A.); (J.-M.L.-G.)
| | - Delphine Beury
- Univ. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, US41-UAR 2014-PLBS, F-59000 Lille, France; (S.C.); (D.B.); (D.H.)
| | - David Hot
- Univ. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, US41-UAR 2014-PLBS, F-59000 Lille, France; (S.C.); (D.B.); (D.H.)
| | - Sébastien Anthérieu
- Univ. Lille, CHU Lille, Institut Pasteur de Lille, ULR 4483-IMPECS—IMPact de l’Environnement Chimique sur la Santé, F-59000 Lille, France; (D.A.); (C.G.); (S.A.); (J.-M.L.-G.)
| | - Jean-Marc Lo-Guidice
- Univ. Lille, CHU Lille, Institut Pasteur de Lille, ULR 4483-IMPECS—IMPact de l’Environnement Chimique sur la Santé, F-59000 Lille, France; (D.A.); (C.G.); (S.A.); (J.-M.L.-G.)
| | - Laurent Dubuquoy
- Univ. Lille, Inserm, CHU Lille, U1286-INFINITE—Institute for Translational Research in Inflammation, F-59000 Lille, France; (M.D.); (C.W.); (L.D.); (D.L.); (C.V.)
| | - David Launay
- Univ. Lille, Inserm, CHU Lille, U1286-INFINITE—Institute for Translational Research in Inflammation, F-59000 Lille, France; (M.D.); (C.W.); (L.D.); (D.L.); (C.V.)
| | - Cécile Vignal
- Univ. Lille, Inserm, CHU Lille, U1286-INFINITE—Institute for Translational Research in Inflammation, F-59000 Lille, France; (M.D.); (C.W.); (L.D.); (D.L.); (C.V.)
| | - Philippe Gosset
- Univ. Lille, CNRS, INSERM, Institut Pasteur de Lille, CHU Lille, Center for Infection and Immunity of Lille (CIIL), UMR9017-U1019, F-59000 Lille, France; (A.O.); (G.K.); (M.P.); (P.G.)
| | - Mathilde Body-Malapel
- Univ. Lille, Inserm, CHU Lille, U1286-INFINITE—Institute for Translational Research in Inflammation, F-59000 Lille, France; (M.D.); (C.W.); (L.D.); (D.L.); (C.V.)
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Zhou X, Ma S, Xu Y, Sun C, Liao J, Song M, Li G, Yuchen L, Chen P, Hu Y, Wang Y, Yu B. Nicotine promotes Staphylococcus aureus-induced osteomyelitis by activating the Nrf2/Slc7a11 signaling axis. Int Immunopharmacol 2024; 135:112223. [PMID: 38772295 DOI: 10.1016/j.intimp.2024.112223] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/13/2023] [Revised: 05/03/2024] [Accepted: 05/05/2024] [Indexed: 05/23/2024]
Abstract
Although smoking is a significant risk factor for osteomyelitis, there is limited experimental evidence that nicotine, a key tobacco constituent, is associated with this condition, leaving its mechanistic implications uncharacterized. This study revealed that nicotine promotes Staphylococcus aureus-induced osteomyelitis by increasing Nrf2 and Slc7a11 expression in vivo and in vitro. Inhibition of Slc7a11 using Erastin augmented bacterial phagocytosis/killing capabilities and fortified antimicrobial responses in an osteomyelitis model. Moreover, untargeted metabolomic analysis demonstrated that Erastin mitigated the effects of nicotine on S. aureus-induced osteomyelitis by altering glutamate/glutathione metabolism. These findings suggest that nicotine aggravates S. aureus-induced osteomyelitis by activating the Nrf2/Slc7a11 signaling pathway and that Slc7a11 inhibition can counteract the detrimental health effects of nicotine.
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Affiliation(s)
- Xuyou Zhou
- Guangdong Provincial Key Laboratory of Bone and Cartilage Regenerative Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China
| | - Sushuang Ma
- Guangdong Provincial Key Laboratory of Bone and Cartilage Regenerative Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Orthopaedics, The Fifth Affiliated Hospital, Southerm Medical University, Guangzhou, China
| | - Yuan Xu
- Guangdong Provincial Key Laboratory of Bone and Cartilage Regenerative Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China
| | - Chongkai Sun
- Guangdong Provincial Key Laboratory of Bone and Cartilage Regenerative Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China
| | - Juncheng Liao
- Guangdong Provincial Key Laboratory of Bone and Cartilage Regenerative Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China
| | - Mingrui Song
- Guangdong Provincial Key Laboratory of Bone and Cartilage Regenerative Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China
| | - Guanzhi Li
- Guangdong Provincial Key Laboratory of Bone and Cartilage Regenerative Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China
| | - Liu Yuchen
- Guangdong Provincial Key Laboratory of Bone and Cartilage Regenerative Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China
| | - Peng Chen
- Guangdong Provincial Key Laboratory of Bone and Cartilage Regenerative Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Orthopedics, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University), Haikou, China
| | - Yanjun Hu
- Guangdong Provincial Key Laboratory of Bone and Cartilage Regenerative Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China
| | - Yutian Wang
- Guangdong Provincial Key Laboratory of Bone and Cartilage Regenerative Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China.
| | - Bin Yu
- Guangdong Provincial Key Laboratory of Bone and Cartilage Regenerative Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China.
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El Hasbani G, E Nassar J, Elsayed Ali AM, Uthman I, Jawad A. The impact of nicotine smoking on spondyloarthritis and rheumatoid arthritis. Reumatismo 2024; 76. [PMID: 38916171 DOI: 10.4081/reumatismo.2024.1572] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/02/2023] [Accepted: 03/18/2024] [Indexed: 06/26/2024] Open
Abstract
OBJECTIVE Nicotine has major side effects on human health through numerous mechanisms, one of which is the alteration of the immune system and its genetic components. Such alteration can be a predisposing factor for autoimmune diseases such as spondyloarthritis (SpA) and rheumatoid arthritis (RA). This review aims to shed light on the effects of nicotine smoking on the pathophysiology, clinical presentation, and management of SpA and RA. METHODS This review looked into the studies, excluding case reports and series, which were cited by PubMed/MEDLINE. RESULTS Patients with established autoimmune conditions may have a different underlying pathophysiology and disease course when exposed to nicotine through cigarette smoking. Through the involvement of several cytokines, endothelial dysfunction, and epigenetic mechanisms, the severity of SpA is more prominent in smokers. The global health status, pain, and fatigue are worse in SpA patients. The evidence on the effect of nicotine smoking on the treatment of SpA is still limited. Nicotine can contribute to RA via the disruption of cellular regulatory activity, inflammatory responses, morphological, physiological, biochemical, and enzymatic responses. As such, smokers with RA have higher disease activity and are more likely to be seropositive through the citrullination of peptides. In addition, these patients are at risk of achieving a suboptimal response to tumor necrosis factor inhibitors. CONCLUSIONS Cigarette smoking can substantially affect the pathophysiology and clinical presentation of patients with SpA and RA. The impact of nicotine on the management of these diseases still needs to be further studied.
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Affiliation(s)
- G El Hasbani
- Department of Medicine, Hartford HealthCare St. Vincent's Medical Center, Bridgeport, CT.
| | - J E Nassar
- Faculty of Medicine, American University of Beirut.
| | | | - I Uthman
- Department of Internal Medicine, American University of Beirut Medical Center.
| | - A Jawad
- Department of Rheumatology, Royal London Hospital.
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Song L, Wu D, Wu J, Zhang J, Li W, Wang C. Investigating causal associations between pneumonia and lung cancer using a bidirectional mendelian randomization framework. BMC Cancer 2024; 24:721. [PMID: 38862880 PMCID: PMC11167773 DOI: 10.1186/s12885-024-12147-3] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/03/2023] [Accepted: 03/19/2024] [Indexed: 06/13/2024] Open
Abstract
BACKGROUND Pneumonia and lung cancer are both major respiratory diseases, and observational studies have explored the association between their susceptibility. However, due to the presence of potential confounders and reverse causality, the comprehensive causal relationships between pneumonia and lung cancer require further exploration. METHODS Genome-wide association study (GWAS) summary-level data were obtained from the hitherto latest FinnGen database, COVID-19 Host Genetics Initiative resource, and International Lung Cancer Consortium. We implemented a bidirectional Mendelian randomization (MR) framework to evaluate the causal relationships between several specific types of pneumonia and lung cancer. The causal estimates were mainly calculated by inverse-variance weighted (IVW) approach. Additionally, sensitivity analyses were also conducted to validate the robustness of the causalty. RESULTS In the MR analyses, overall pneumonia demonstrated a suggestive but modest association with overall lung cancer risk (Odds ratio [OR]: 1.21, 95% confidence interval [CI]: 1.01 - 1.44, P = 0.037). The correlations between specific pneumonia types and overall lung cancer were not as significant, including bacterial pneumonia (OR: 1.07, 95% CI: 0.91 - 1.26, P = 0.386), viral pneumonia (OR: 1.00, 95% CI: 0.95 - 1.06, P = 0.891), asthma-related pneumonia (OR: 1.18, 95% CI: 0.92 - 1.52, P = 0.181), and COVID-19 (OR: 1.01, 95% CI: 0.78 - 1.30, P = 0.952). Reversely, with lung cancer as the exposure, we observed that overall lung cancer had statistically crucial associations with bacterial pneumonia (OR: 1.08, 95% CI: 1.03 - 1.13, P = 0.001) and viral pneumonia (OR: 1.09, 95% CI: 1.01 - 1.19, P = 0.037). Sensitivity analysis also confirmed the robustness of these findings. CONCLUSION This study has presented a systematic investigation into the causal relationships between pneumonia and lung cancer subtypes. Further prospective study is warranted to verify these findings.
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Affiliation(s)
- Lujia Song
- Department of Pulmonary and Critical Care Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, Targeted Tracer Research and Development Laboratory, Med-X Center for Manufacturing, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China
| | - Dongsheng Wu
- Department of Thoracic Surgery, Institute of Thoracic Oncology, West China Hospital, Sichuan University, Chengdu, Sichuan, China
| | - Jiayang Wu
- Department of Pulmonary and Critical Care Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, Targeted Tracer Research and Development Laboratory, Med-X Center for Manufacturing, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China
| | - Jiexi Zhang
- Chengdu Medical College, Chengdu, Sichuan, China
| | - Weimin Li
- Department of Pulmonary and Critical Care Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, Targeted Tracer Research and Development Laboratory, Med-X Center for Manufacturing, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
| | - Chengdi Wang
- Department of Pulmonary and Critical Care Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, Targeted Tracer Research and Development Laboratory, Med-X Center for Manufacturing, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
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Zięba S, Maciejczyk M, Antonowicz B, Porydzaj A, Szuta M, Lo Giudice G, Lo Giudice R, Krokosz S, Zalewska A. Comparison of smoking traditional, heat not burn and electronic cigarettes on salivary cytokine, chemokine and growth factor profile in healthy young adults-pilot study. Front Physiol 2024; 15:1404944. [PMID: 38915777 PMCID: PMC11194668 DOI: 10.3389/fphys.2024.1404944] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/21/2024] [Accepted: 05/28/2024] [Indexed: 06/26/2024] Open
Abstract
Objective: Smoking is the cause of numerous oral pathologies. The aim of the study was to evaluate the effect of smoking traditional cigarettes, e-cigarettes, and heat-not-burn products on the content of salivary cytokines, chemokines, and growth factors in healthy young adults. Design: Three groups of twenty-five smokers each as well as a control group matched in terms of age, gender, and oral status were enrolled in the study. In unstimulated saliva collected from study groups and participants from the control group, the concentrations of cytokines, chemokines, and growth factors were assessed by Bio-Plex® Multiplex System. Results: We demonstrated that smoking traditional cigarettes is responsible for increasing the level of IFN-γ compared to non-smokers and new smoking devices users in unstimulated saliva in the initial period of addiction. Furthermore, e-cigarettes and heat-not-burn products appear to have a similar mechanism of affecting the immune response system of unstimulated saliva, leading to inhibition of the local inflammatory response in the oral cavity. Conclusion: Smoking traditional cigarettes as well as e-cigarettes and heat-not-burn products is responsible for changes of the local immune response in saliva. Further research is necessary to fill the gap in knowledge on the effect of new smoking devices on the oral cavity immune system.
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Affiliation(s)
- Sara Zięba
- Doctoral Studies, Medical University of Bialystok, Bialystok, Poland
| | - Mateusz Maciejczyk
- Department of Hygiene, Epidemiology, and Ergonomics, Medical University of Bialystok, Bialystok, Poland
| | - Bożena Antonowicz
- Department of Dental Surgery, Medical University in Bialystok, Bialystok, Poland
| | - Aleksandra Porydzaj
- Student Research Group of Department of Restorative Dentistry, Medical University of Bialystok, Bialystok, Poland
| | - Mariusz Szuta
- Department of Oral Surgery, Jagiellonian University Medical College, Cracow, Poland
| | - Giuseppe Lo Giudice
- Department of Biomedical and Dental Sciences and Morphofunctional Imaging, Messina University, Messina, Italy
| | - Roberto Lo Giudice
- Department of Human Pathology of the Adult and Evolutive Age. G. Barresi, Messina University, Messina, Italy
| | - Stanisław Krokosz
- Student Research Group of Department of Restorative Dentistry, Medical University of Bialystok, Bialystok, Poland
| | - Anna Zalewska
- Independent Laboratory of Experimental Dentistry, Medical University of Bialystok, Bialystok, Poland
- Department of Restorative Dentistry, Medical University of Bialystok, Bialystok, Poland
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Sigvardsson I, Ludvigsson J, Andersson B, Størdal K, Mårild K. Tobacco Smoke Exposure in Early Childhood and Later Risk of Inflammatory Bowel Disease: A Scandinavian Birth Cohort Study. J Crohns Colitis 2024; 18:661-670. [PMID: 38329478 PMCID: PMC11140631 DOI: 10.1093/ecco-jcc/jjae020] [Citation(s) in RCA: 4] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/26/2023] [Indexed: 02/09/2024]
Abstract
OBJECTIVES To examine the association between early-life smoking exposure and later risk of inflammatory bowel disease [IBD]. METHODS We followed 115663 participants from the Norwegian Mother, Father and Child [MoBa] and All Babies in Southeast Sweden [ABIS] cohorts from birth [1997-2009] through 2021. IBD was identified through national patient registers. Validated questionnaire data defined maternal smoking during pregnancy, maternal environmental tobacco smoke [ETS] exposure during pregnancy, and child ETS exposure by ages 12 and 36 months. Cox regression was used to estimate adjusted hazard ratios [aHRs] for sex, maternal age, education level, parental IBD, and origin. Cohort-specific estimates were pooled using a random-effects model. RESULTS During 1 987 430 person-years of follow-up, 444 participants developed IBD [ABIS, 112; MoBa, 332]. Any vs no maternal smoking during pregnancy yielded a pooled aHR of 1.30 [95% CI = 0.97-1.74] for offspring IBD. Higher level of maternal smoking during pregnancy (compared with no smoking, average ≥6 cigarettes/day: pooled aHR = 1.60 [95% CI = 1.08-2.38]) was associated with offspring IBD, whereas a lower smoking level was not (average 1-5 cigarettes/day: pooled aHR = 1.09 [95% CI = 0.73-1.64]). Child ETS exposure in the first year of life was associated with later IBD (any vs no ETS, pooled aHR = 1.32 [95% CI = 1.03-1.69]). Estimates observed for child ETS exposure by 36 months were similar but not statistically significant. CONCLUSIONS In this prospective Scandinavian cohort study, children exposed to higher levels of maternal smoking during pregnancy or ETS during the first year of life were at increased risk of later IBD.
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Affiliation(s)
- Ida Sigvardsson
- Department of Pediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, Gothenburg, Sweden
| | - Johnny Ludvigsson
- Crown Princess Victoria Children’s Hospital, Region Östergötland, Linköping, Sweden
- Division of Pediatrics, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden
| | - Björn Andersson
- Bioinformatics and Data Centre, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
| | - Ketil Størdal
- Department of Pediatric Research, Faculty of Medicine, University of Oslo, Oslo, Norway
- Children’s Center, Oslo University Hospital, Oslo, Norway
| | - Karl Mårild
- Department of Pediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, Gothenburg, Sweden
- Department of Pediatrics, Queen Silvia Children’s Hospital, Gothenburg, Sweden
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Li J, Yang Z, Yuan W, Bao Z, Li MD. Heme Metabolism Mediates the Effects of Smoking on Gut Microbiome. Nicotine Tob Res 2024; 26:742-751. [PMID: 37875417 DOI: 10.1093/ntr/ntad209] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/13/2023] [Revised: 09/12/2023] [Accepted: 10/20/2023] [Indexed: 10/26/2023]
Abstract
INTRODUCTION The number of smokers worldwide increased greatly during the past decades and reached 1.14 billion in 2019, becoming a leading risk factor for human health. Tobacco smoking has wide effects on human genetics, epigenetics, transcriptome, and gut microbiome. Although many studies have revealed effects of smoking on host transcriptome, research on the relationship between smoking, host gene expression, and the gut microbiome is limited. AIMS AND METHODS We first explored transcriptome and metagenome profile differences between smokers and nonsmokers. To evaluate the relationship between host gene expression and gut microbiome, we then applied bidirectional mediation analysis to infer causal relationships between smoking, gene expression, and gut microbes. RESULTS Metagenome and transcriptome analyses revealed 71 differential species and 324 differential expressed genes between smokers and nonsmokers. With smoking as an exposure variable, we identified 272 significant causal relationships between gene expression and gut microbes, among which there were 247 genes that mediate the effect of smoking on gut microbes. Pathway-based enrichment analysis showed that these genes were significantly enriched in heme metabolic pathway, which mainly mediated the changes of Bacteroides finegoldii and Lachnospiraceae bacterium 9_1_43BFAA. Additionally, by performing metabolome data analysis in the Integrated Human Microbiome Project (iHMP) database, we verified the correlation between the intermediate products of the heme metabolism pathway (porphobilinogen, bilirubin, and biliverdin) and gut microbiome. CONCLUSIONS By investigating the bidirectional interaction between smoking-related host gene expression and gut microbes, this study provided evidence for the mediation of smoking on gut microbes through co-involvement or interaction of heme metabolism. IMPLICATIONS By comparing the metagenome and transcriptome sequencing profiles between 34 smokers and 33 age- and gender-matched nonsmokers, we are the first to reveal causal relationships among tobacco smoking, host gene expression, and gut microbes. These findings offer insight into how smoking affects gut microbes through host gene expression and metabolism, which highlights the importance of heme metabolism in modulating the effects of smoking on gut microbiome.
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Affiliation(s)
- Jingjing Li
- State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
- Institute of Biomedical Big Data, School of Ophthalmology and Optometry and Eye Hospital, School of Biomedical Engineering, Wenzhou Medical University, Wenzhou, China
| | - Zhongli Yang
- State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
| | - Wenji Yuan
- State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
| | - Zhiwei Bao
- State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
| | - Ming D Li
- State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
- Research Center for Air Pollution and Health, Zhejiang University, Hangzhou, China
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Qi X, Fu J, Liu J, Wu X, Zheng X, Wang S. Association between secondhand smoke exposure and rheumatoid arthritis in US never-smoking adults: a cross-sectional study from NHANES. Sci Rep 2024; 14:11061. [PMID: 38745032 PMCID: PMC11094008 DOI: 10.1038/s41598-024-61950-2] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/06/2024] [Accepted: 05/12/2024] [Indexed: 05/16/2024] Open
Abstract
While smoking is widely acknowledged as a risk factor for rheumatoid arthritis (RA), the connection between secondhand smoke (SHS) exposure and RA in never-smoking adults remains limited and inconsistent. This study aims to explore and quantify this association using serum cotinine levels. We conducted a cross-sectional study with 14,940 adults who self-report as never smokers, using National Health and Nutrition Examination Survey data from 1999 to 2018. Based on previous literature, SHS exposure was categorized into four groups according to serum cotinine levels. Compared to individuals in the unexposed group (serum cotinine < 0.05 ng/mL), the adjusted odds ratio (OR) for RA was 1.37 (95% CI 1.14-1.64, p = 0.001) in the low exposure group (serum cotinine at 0.05 to 0.99 ng/mL) after adjusting for covariates. However, no significant association was found in the moderate exposure group (serum cotinine at 1 to 10 ng/mL) or the heavy exposure group (serum cotinine ≥ 10 ng/mL). Furthermore, we detected a non-linear, positively saturated correlation between the cotinine levels after log2 transformation and RA, with a turning point at approximately - 2.756 ng/mL (OR = 1.163, 95% CI 1.073-1.261, p = 0.0002). The stability of the results was confirmed by subgroup analysis.
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Affiliation(s)
- Xiaogang Qi
- Department of Orthopedics, The Second Hospital of Shanxi Medical University, Taiyuan, 030000, China
| | - Junwen Fu
- Department of Orthopedics, Yangquan Coal Group General Hospital, Yangquan, 045000, China
| | - Jiaming Liu
- Pain Department, Yangquan First People's Hospital, Yangquan, 045000, China
| | - Xupeng Wu
- Department of Neurology, Changzhi Medical College Affiliated Heping Hospital, Changzhi, 046000, China
| | - Xin Zheng
- Department of Cardiovascular Medicine, Yangquan First People's Hospital, Yangquan, 045000, China
| | - Shaowei Wang
- Department of Orthopedics, The Second Hospital of Shanxi Medical University, Taiyuan, 030000, China.
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Franco-García JM, Castillo-Paredes A, Rodríguez-Redondo Y, Carlos-Vivas J, García-Carrillo RM, Denche-Zamorano Á. Greater physical activity levels are associated with lower prevalence of tumors and risk of cancer in Spanish population: A cross-sectional study. Heliyon 2024; 10:e29191. [PMID: 38623236 PMCID: PMC11016703 DOI: 10.1016/j.heliyon.2024.e29191] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/28/2023] [Revised: 03/31/2024] [Accepted: 04/02/2024] [Indexed: 04/17/2024] Open
Abstract
Cancer is a leading cause of death worldwide and insufficient physical activity is a significant risk factor. This study analyzed the tumor prevalence based on sex, age, smoking, BMI, and physical activity level (PAL) in the Spanish people. Data from the Spanish National Health Survey (ENSE) was used, comprising a sample of 17,704 people diagnosed with malignant tumors. The findings revealed compelling associations (P < 0.001) between all variables examined and the prevalence of malignant tumors. Notably, women exhibited a higher prevalence than men (P < 0.05). Furthermore, individuals classified as obese displayed a greater prevalence of tumors than those within the normal weight range (P < 0.05). The analysis also showed that the inactive group had a higher prevalence of malignant tumors than the active group (P < 0.05). This study identified significant dependency relationships (P < 0.001) between PAL and the various population groups examined. Additionally, the general population analyzed in the ENSE2017 study demonstrated a reduced risk of developing malignant tumors among the active (P < 0.05) and very active groups (P < 0.05) compared to the inactive group. This risk reduction was consistently observed across different subgroups, including men, women, specific age groups, smoking, and BMI categories (P < 0.05). This study highlighted the importance of regular physical activity in reducing the risk and prevalence of malignant tumors in the Spanish population. These findings underscore the critical role of engaging in physical activity as a protective measure against cancer. Encouraging individuals to adopt an active lifestyle could significantly contribute to cancer prevention efforts and promote overall well-being.
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Affiliation(s)
- Juan Manuel Franco-García
- Health, Economy, Motricity and Education (HEME) Research Group, Faculty of Sport Sciences, University of Extremadura, Cáceres, 10003, Spain
| | - Antonio Castillo-Paredes
- Grupo AFySE, Investigación en Actividad Física y Salud Escolar, Escuela de Pedagogía en Educación Física, Facultad de Educación, Universidad de Las Américas, Santiago, 8370040, Chile
| | - Yeray Rodríguez-Redondo
- Social Impact and Innovation in Health (InHEALTH), University of Extremadura, 06810, Mérida, Spain
| | - Jorge Carlos-Vivas
- Physical Activity for Education, Performance and Health (PAEPH) Research Group, Faculty of Sport Sciences, University of Extremadura, 10003, Cáceres, Spain
| | - Rosa María García-Carrillo
- Health, Economy, Motricity and Education (HEME) Research Group, Faculty of Sport Sciences, University of Extremadura, Cáceres, 10003, Spain
| | - Ángel Denche-Zamorano
- Promoting a Healthy Society (PHeSO) Research Group, Faculty of Sport Sciences, University of Extremadura, 10003, Cáceres, Spain
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Ndeke JM, Klaunig JE, Commodore S. Nicotine or marijuana vaping exposure during pregnancy and altered immune responses in offspring. JOURNAL OF ENVIRONMENTAL EXPOSURE ASSESSMENT 2024; 3:10.20517/jeea.2024.03. [PMID: 38840831 PMCID: PMC11152453 DOI: 10.20517/jeea.2024.03] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Subscribe] [Scholar Register] [Indexed: 06/07/2024]
Abstract
Electronic nicotine delivery systems (ENDS) - which include electronic cigarettes or e-cigarettes, or simply e-cigs, and marijuana vaping have become increasingly popular. ENDS devices have been established as one of the tobacco quit methods and promoted to be safer compared to traditional tobacco cigarettes. Emerging evidence demonstrates that e-cigarette and marijuana vape use can be harmful, with potential associations with cancer. Herein, we summarize the level of evidence to date for altered immune response, with a focus on cancer risks in the offspring after maternal use of, or aerosol exposures from, ENDS or marijuana vape during pregnancy. From 27 published articles retrieved from PubMed, we sought to find out identified carcinogens in ENDS aerosols and marijuana vapor, which cross the placental barrier and can increase cancer risk in the offspring. Carcinogens in vaping aerosols include aldehydes, metals, tobacco-specific nitrosamines, tobacco alkaloids, polycyclic aromatic hydrocarbons, and volatile organic compounds. Additionally, there was only one passive vaping exposure case study on a human fetus, which noted that glycerol, aluminum, chromium, nickel, copper, zinc, selenium, and lead crossed from the mother to the offspring's cord blood. The carcinogens (metals) in that study were at lower concentrations compared to the mother's biological matrices. Lastly, we observed that in utero exposures to ENDS-associated chemicals can occur in vital organs such as the lungs, kidneys, brain, bladder, and heart. Any resulting DNA damage increases the risk of tumorigenesis. Future epidemiological studies are needed to examine the effects of passive aerosol exposures from existing and emerging electronic nicotine and marijuana products on developing offspring to cancer.
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Affiliation(s)
- Jonas M. Ndeke
- Department of Epidemiology and Biostatistics, Indiana University School of Public Health, Bloomington, IN 47405, USA
| | - James E. Klaunig
- Department of Environmental and Occupational Health, Indiana University School of Public Health, Bloomington, IN 47408, USA
| | - Sarah Commodore
- Department of Environmental and Occupational Health, Indiana University School of Public Health, Bloomington, IN 47408, USA
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Zhang L, Xu J, Li Y, Meng F, Wang W. Smoking on the risk of acute respiratory distress syndrome: a systematic review and meta-analysis. Crit Care 2024; 28:122. [PMID: 38616271 PMCID: PMC11017665 DOI: 10.1186/s13054-024-04902-6] [Citation(s) in RCA: 2] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/18/2024] [Accepted: 04/03/2024] [Indexed: 04/16/2024] Open
Abstract
BACKGROUND The relationship between smoking and the risk of acute respiratory distress syndrome (ARDS) has been recognized, but the conclusions have been inconsistent. This systematic review and meta-analysis investigated the association between smoking and ARDS risk in adults. METHODS The PubMed, EMBASE, Cochrane Library, and Web of Science databases were searched for eligible studies published from January 1, 2000, to December 31, 2023. We enrolled adult patients exhibiting clinical risk factors for ARDS and smoking condition. Outcomes were quantified using odds ratios (ORs) for binary variables and mean differences (MDs) for continuous variables, with a standard 95% confidence interval (CI). RESULTS A total of 26 observational studies involving 36,995 patients were included. The meta-analysis revealed a significant association between smoking and an increased risk of ARDS (OR 1.67; 95% CI 1.33-2.08; P < 0.001). Further analysis revealed that the associations between patient-reported smoking history and ARDS occurrence were generally similar to the results of all the studies (OR 1.78; 95% CI 1.38-2.28; P < 0.001). In contrast, patients identified through the detection of tobacco metabolites (cotinine, a metabolite of nicotine, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), a metabolite of tobacco products) showed no significant difference in ARDS risk (OR 1.19; 95% CI 0.69-2.05; P = 0.53). The smoking group was younger than the control group (MD - 7.15; 95% CI - 11.58 to - 2.72; P = 0.002). Subgroup analysis revealed that smoking notably elevated the incidence of ARDS with extrapulmonary etiologies (OR 1.85; 95% CI 1.43-2.38; P < 0.001). Publication bias did not affect the integrity of our conclusions. Sensitivity analysis further reinforced the reliability of our aggregated outcomes. CONCLUSIONS There is a strong association between smoking and elevated ARDS risk. This emphasizes the need for thorough assessment of patients' smoking status, urging healthcare providers to vigilantly monitor individuals with a history of smoking, especially those with additional extrapulmonary risk factors for ARDS.
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Affiliation(s)
- Lujia Zhang
- Institute of Respiratory and Critical Care Medicine, The First Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, Liaoning, China
| | - Jiahuan Xu
- Institute of Respiratory and Critical Care Medicine, The First Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, Liaoning, China
| | - Yue Li
- Institute of Respiratory and Critical Care Medicine, First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China
| | - Fanqi Meng
- Institute of Respiratory and Critical Care Medicine, The First Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, Liaoning, China
| | - Wei Wang
- Institute of Respiratory and Critical Care Medicine, The First Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, Liaoning, China.
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Chen N, Fong DYT, Wong JYH. Health and economic burden of low back pain and rheumatoid arthritis attributable to smoking in 192 countries and territories in 2019. Addiction 2024; 119:677-685. [PMID: 38105035 DOI: 10.1111/add.16404] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/24/2022] [Accepted: 10/30/2023] [Indexed: 12/19/2023]
Abstract
BACKGROUND AND AIMS Smoking is a risk factor for low back pain (LBP) and rheumatoid arthritis (RA). We aimed to estimate the global health and economic burden of LBP and RA attributable to smoking. DESIGN This was a cross-sectional study. SETTING The study was conducted in 192 countries and territories. CASES Prevalent cases of LBP and RA were used, extracted from the Global Burden of Diseases, Injuries and Risk Factors Study 2019 data repositories. MEASUREMENTS Smoking-attributable health and economic burden was estimated with the population-attributable fraction method. Smoking-attributable prevalence of LBP and RA and health-care costs were estimated for patients of all ages, whereas years lived with disability (YLDs) and productivity losses due to morbidity were estimated for patients aged 15-84 years. Uncertainty intervals (UIs) of the results were obtained by repeating the analysis with the lower and upper bounds of all input variables. FINDINGS Globally, smoking accounted for 84.5 million (UI = 56.7-120.2 million) prevalent cases of LBP, 1.8 million (UI = 0.5-3.4 million) prevalent cases of RA and 11.3 million (UI = 6.2-18.5 million) YLDs, which represented 1.5% of all-cause YLDs in the working-age population aged 15-84 years in 2019. Health-care costs and productivity losses of smoking-attributable LBP and RA cost the global economy purchasing-power parity $326.0 billion (UI = $184.0-521.4 billion), representing 0.2% of the global gross domestic product. Specifically, smoking accounted for $65.8 billion (UI = $38.0-101.2 billion) in health-care costs world-wide, with more than half [$39.8 billion (UI = $23.1-61.3 billion), 60.6%] borne by the public sector. Smoking also contributed to $260.3 billion (UI = $146.0-420.3 billion) in productivity losses globally. Approximately 60.0% of the global YLDs were observed in middle-income countries, whereas 84.4% of health-care costs and 72.7% of productivity losses were borne by high-income countries. CONCLUSIONS Globally, in 2019, smoking accounted for more than 11.0 million years lived with disability and purchasing-power parity $326.0 billion in economic losses due to low back pain and rheumatoid arthritis. Middle-income countries suffered more morbidity, whereas high-income countries experienced larger economic losses.
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Affiliation(s)
- Ningjing Chen
- School of Nursing, Putian University, Putian, China
- School of Nursing, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China
| | - Daniel Yee Tak Fong
- School of Nursing, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China
| | - Janet Yuen Ha Wong
- School of Nursing, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China
- School of Nursing and Health Studies, Hong Kong Metropolitan University, Hong Kong, China
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Abellán Alemán J, Sabaris RC, Pardo DE, García Donaire JA, Romanos FG, Iriso JI, Penagos LM, Iglesias LJN, de Salinas APM, Pérez-Monteoliva NRR, Lezcano PSR, Saborido MT, Roca FV. Documento de consenso sobre tabaquismo y riesgo vascular. HIPERTENSION Y RIESGO VASCULAR 2024; 41 Suppl 1:S1-S85. [PMID: 38729667 DOI: 10.1016/s1889-1837(24)00075-8] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 05/12/2024]
Abstract
Consensus statement on smoking and vascular risk About 22% of the Spanish population are daily smokers. Men are more likely to smoke than women. In Spain, women between 15-25 years of age smoke as much or more than men. Every smoker should be assessed for: physical dependence on nicotine (Fagerström test), social and psychological dependence (Glover Nilsson test), level of motivation to quit (Richmond test), probability of therapy success (Henri-Mondor and Michael-Fiore tests), and stage of behavioral change development (Prochaska and DiClementi). Advice on smoking cessation is highly cost-effective and should always be provided. Smoking is an enhancer of cardiovascular risk because it acts as a pathogen agent in the development of arteriosclerosis and is associated with ischemic heart disease, stroke, and peripheral artery disease. Smoking increases the risk of chronic lung diseases (COPD) and is related to cancers of the lung, female genitalia, larynx, oropharynx, bladder, mouth, esophagus, liver and biliary tract, and stomach, among others. Combined oral contraceptives should be avoided in women smokers older than 35 years of age due to the risk of thromboembolism. In smoking cessation, the involvement of physicians, nurses, psychologists, etc. is important, and their multidisciplinary collaboration is needed. Effective pharmacological treatments for smoking cessation are available. Combined treatments are recommended when smoker's dependence is high. For individuals who are unable to quit smoking, a strategy based on tobacco damage management with a total switch to smokeless products could be a less dangerous alternative for their health than continuing to smoke.
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Affiliation(s)
- José Abellán Alemán
- Sociedad Murciana de Hipertensión Arterial y Riesgo Cardiovascular, Cátedra de Riesgo Cardiovascular, Universidad Católica de Murcia, Murcia, España.
| | - Rafael Crespo Sabaris
- Sociedad Riojana de Hipertensión y Riesgo Vascular, Centro de Salud de Entrena, La Rioja, España
| | - Daniel Escribano Pardo
- Sociedad Aragonesa de Hipertensión y Riesgo Vascular, Centro de Salud Oliver, Zaragoza, España
| | - José Antonio García Donaire
- Sociedad Española de Hipertensión, Unidad de Hipertensión, Servicio de Medicina Interna, Hospital Clínico Universitario San Carlos, Madrid, España
| | - Fernando García Romanos
- Sociedad de Hipertensión y Riesgo Vascular de las Illes Balears, Centro de Salud Santa Catalina, Palma de Mallorca, España
| | - Jesús Iturralde Iriso
- Sociedad Vasca de Hipertensión y Riesgo Vascular, Centro de Salud la Habana-Cuba, Vitoria-Gasteiz, España
| | - Luis Martín Penagos
- Sociedad Cántabra de Hipertensión y Riesgo Vascular, Servicio de Nefrología, Hospital Universitario Marqués de Valdecilla, Santander, España
| | - L Javier Nieto Iglesias
- Sociedad Castilla-La Mancha de Hipertensión y Riesgo Vascular, Unidad de Hipertensión y Riesgo Vascular, Servicio de Nefrología, Hospital General Universitario de Ciudad Real, Ciudad Real, España
| | - Alfonso Pobes Martínez de Salinas
- Sociedad Asturiana de Hipertensión y Riesgo Vascular, Área de Gestión Clínica, Interáreas de Nefrología VII y VIII del SESPA, Asturias, España
| | | | - Pablo Sánchez-Rubio Lezcano
- Sociedad Aragonesa de Hipertensión y Riesgo Vascular, Servicio de Medicina Interna, Hospital General Universitario San Jorge, Huesca, España
| | - Maribel Troya Saborido
- Sociedad Catalana de Hipertensión y Riesgo Vascular, Servicio de Nefrología, Hospital Universitari Germans Trias i Pujol, Badalona, Barcelona, España
| | - Francisco Valls Roca
- Sociedad Valenciana de Hipertensión y Riesgo Vascular, Centro de Salud de Beniganim, Valencia, España
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Fukuyama S, Shoemaker JE, Zhao D, Nagajima N, Tomita Y, Maemura T, da Silva Lopes TJ, Watanabe T, Yamayoshi S, Hasegawa H, Kawaoka Y. Attenuation of A(H7N9) influenza virus infection in mice exposed to cigarette smoke. NPJ VIRUSES 2024; 2:16. [PMID: 40295873 PMCID: PMC11721123 DOI: 10.1038/s44298-024-00026-4] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Received: 10/22/2023] [Accepted: 03/04/2024] [Indexed: 04/30/2025]
Abstract
Influenza A(H7N9) virus showed high pathogenicity in humans when it emerged in 2013. Cigarette smoke (CS) causes pulmonary diseases including bronchitis, emphysema, and lung cancer. Although habitual smoking is thought to increase the risk of severe seasonal influenza virus infection, its effect on A(H7N9) virus infection is poorly understood. Here, we employed a mouse model of long-term exposure to CS to investigate the effect of CS on the pathogenicity of A(H7N9) virus infection. Unexpectedly, body weight loss for mice exposed to CS was milder than that for mock-treated mice upon A(H7N9) virus infection. CS exposure improved the survival rate of A(H7N9) virus-infected mice even though virus titers and pathological changes in the lungs were not significantly different between CS-exposed and control mice. Microarray analysis showed that CS-exposure activates cytokine/chemokine activity, immune response, and cell cycle activities that resemble reactivities against A(H7N9) virus infection. Therefore, under conditions where cytokine and chemokine expression in the lungs is already high due to CS exposure, the enhanced expression of cytokines and chemokines caused by A(H7N9) virus infection might be less harmful to the organs compared to the rapid increase in cytokine and chemokine expression in the air-exposed mice due to the infection. CS may thus induce immunoregulatory effects that attenuate severe pulmonary disease during A(H7N9) virus infection. However, these findings do not support CS exposure due to its many other proven negative health effects.
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Affiliation(s)
- Satoshi Fukuyama
- Division of Virology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan
| | - Jason E Shoemaker
- Division of Virology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan
- Department of Chemical and Petroleum Engineering, Swanson School of Engineering, University of Pittsburgh, Pittsburgh, PA, USA
- Department of Computational & Systems Biology, University of Pittsburgh, Pittsburgh, PA, USA
| | - Dongming Zhao
- Division of Virology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan
| | - Noriko Nagajima
- Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan
| | - Yuriko Tomita
- Division of Virology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan
| | - Tadashi Maemura
- Division of Virology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan
| | - Tiago Jose da Silva Lopes
- Division of Virology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan
- Influenza Virus Research Center, National Institute of Infectious Diseases, Tokyo, Japan
| | - Tokiko Watanabe
- Division of Virology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan
- Department of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan
- Center for Advanced Modalities and DDS, Osaka University, Osaka, Japan
- Center for Infectious Disease Education and Research, Osaka University, Osaka, Japan
| | - Seiya Yamayoshi
- Division of Virology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan
- Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI, USA
- International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo, Tokyo, Japan
| | - Hideki Hasegawa
- Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan
- Influenza Virus Research Center, National Institute of Infectious Diseases, Tokyo, Japan
| | - Yoshihiro Kawaoka
- Division of Virology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan.
- Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI, USA.
- International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
- The Research Center for Global Viral Diseases, National Center for Global Health and Medicine Research Institute, Tokyo, Japan.
- The University of Tokyo, Pandemic Preparedness, Infection, and Advanced Research Center, Tokyo, Japan.
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Kjerulff B, Dowsett J, Jacobsen RL, Gladov J, Larsen MH, Lundgaard AT, Banasik K, Westergaard D, Mikkelsen S, Dinh KM, Hindhede L, Kaspersen KA, Schwinn M, Juul A, Poulsen B, Lindegaard B, Pedersen CB, Sabel CE, Bundgaard H, Nielsen HS, Møller JA, Boldsen JK, Burgdorf KS, Kessing LV, Handgaard LJ, Thørner LW, Didriksen M, Nyegaard M, Grarup N, Ødum N, Johansson PI, Jennum P, Frikke-Schmidt R, Berger SS, Brunak S, Jacobsen S, Hansen TF, Lundquist TK, Hansen T, Sørensen TL, Sigsgaard T, Nielsen KR, Bruun MT, Hjalgrim H, Ullum H, Rostgaard K, Sørensen E, Pedersen OB, Ostrowski SR, Erikstrup C. Lifestyle and demographic associations with 47 inflammatory and vascular stress biomarkers in 9876 blood donors. COMMUNICATIONS MEDICINE 2024; 4:50. [PMID: 38493237 PMCID: PMC10944541 DOI: 10.1038/s43856-024-00474-2] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/31/2023] [Accepted: 03/04/2024] [Indexed: 03/18/2024] Open
Abstract
BACKGROUND The emerging use of biomarkers in research and tailored care introduces a need for information about the association between biomarkers and basic demographics and lifestyle factors revealing expectable concentrations in healthy individuals while considering general demographic differences. METHODS A selection of 47 biomarkers, including markers of inflammation and vascular stress, were measured in plasma samples from 9876 Danish Blood Donor Study participants. Using regression models, we examined the association between biomarkers and sex, age, Body Mass Index (BMI), and smoking. RESULTS Here we show that concentrations of inflammation and vascular stress biomarkers generally increase with higher age, BMI, and smoking. Sex-specific effects are observed for multiple biomarkers. CONCLUSION This study provides comprehensive information on concentrations of 47 plasma biomarkers in healthy individuals. The study emphasizes that knowledge about biomarker concentrations in healthy individuals is critical for improved understanding of disease pathology and for tailored care and decision support tools.
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Affiliation(s)
- Bertram Kjerulff
- Department of Clinical Immunology, Aarhus University Hospital, Aarhus, Denmark.
- Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
- BERTHA Big Data Centre for Environment and Health, Aarhus University, Aarhus, Denmark.
| | - Joseph Dowsett
- Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
| | - Rikke Louise Jacobsen
- Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
| | - Josephine Gladov
- Department of Clinical Immunology, Aarhus University Hospital, Aarhus, Denmark
- Department of Clinical Medicine, Aarhus University, Aarhus, Denmark
- BERTHA Big Data Centre for Environment and Health, Aarhus University, Aarhus, Denmark
| | - Margit Hørup Larsen
- Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
| | - Agnete Troen Lundgaard
- Translational Disease Systems Biology, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
| | - Karina Banasik
- Translational Disease Systems Biology, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
| | - David Westergaard
- Translational Disease Systems Biology, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
| | - Susan Mikkelsen
- Department of Clinical Immunology, Aarhus University Hospital, Aarhus, Denmark
| | - Khoa Manh Dinh
- Department of Clinical Immunology, Aarhus University Hospital, Aarhus, Denmark
| | - Lotte Hindhede
- Department of Clinical Immunology, Aarhus University Hospital, Aarhus, Denmark
| | - Kathrine Agergård Kaspersen
- Department of Clinical Immunology, Aarhus University Hospital, Aarhus, Denmark
- BERTHA Big Data Centre for Environment and Health, Aarhus University, Aarhus, Denmark
| | - Michael Schwinn
- Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
| | - Anders Juul
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Department of Growth and Reproduction, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark
- International Center for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
| | - Betina Poulsen
- Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
| | - Birgitte Lindegaard
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Department of Pulmonary and Infectious Diseases, Copenhagen University Hospital-North Zealand, Hillerød, Denmark
| | - Carsten Bøcker Pedersen
- BERTHA Big Data Centre for Environment and Health, Aarhus University, Aarhus, Denmark
- National Centre for Register-based Research, Aarhus BSS, Aarhus University, Aarhus, Denmark
| | - Clive Eric Sabel
- BERTHA Big Data Centre for Environment and Health, Aarhus University, Aarhus, Denmark
- Department of Public Health, Aarhus University, DK-8000, Aarhus, Denmark
- School of Geography, Earth and Environmental Sciences, University of Plymouth, Plymouth, PL4 8AA, UK
| | - Henning Bundgaard
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- The Heart Center, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark
| | - Henriette Svarre Nielsen
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Recurrent Pregnancy Loss Unit, Capital Region, Copenhagen University Hospitals, Hvidovre and Rigshospitalet, Copenhagen, Denmark
- Department of Obstetrics and Gynecology, Copenhagen University Hospital, Hvidovre, Denmark
| | - Janne Amstrup Møller
- Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
| | - Jens Kjærgaard Boldsen
- Department of Clinical Immunology, Aarhus University Hospital, Aarhus, Denmark
- BERTHA Big Data Centre for Environment and Health, Aarhus University, Aarhus, Denmark
| | - Kristoffer Sølvsten Burgdorf
- Translational Disease Systems Biology, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
| | - Lars Vedel Kessing
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Copenhagen Affective Disorder Research Center (CADIC), Psychiatric Center Copenhagen, Copenhagen, Denmark
| | - Linda Jenny Handgaard
- Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
| | - Lise Wegner Thørner
- Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
| | - Maria Didriksen
- Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
| | - Mette Nyegaard
- Department of Health Science and Technology, Aalborg University, Aalborg, Denmark
| | - Niels Grarup
- Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
| | - Niels Ødum
- LEO Foundation Skin Immunology Research Center, Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark
| | - Pär I Johansson
- Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
- Department of Obstetrics and Gynecology, Copenhagen University Hospital, Hvidovre, Denmark
| | - Poul Jennum
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Danish Center for Sleep Medicine, Department of Clinical Neurophysiology, Rigshospitalet, Copenhagen, Denmark
| | - Ruth Frikke-Schmidt
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Department of Clinical Biochemistry, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark
| | - Sanne Schou Berger
- Centre for Diagnostics, DTU Health Technology, Technical University of Denmark, 2800, Kgs. Lyngby, Denmark
| | - Søren Brunak
- Translational Disease Systems Biology, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
| | - Søren Jacobsen
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Copenhagen Lupus and Vasculitis Clinic, Center for Rheumatology and Spine Diseases, Rigshospitalet, Copenhagen, Denmark
| | - Thomas Folkmann Hansen
- Translational Disease Systems Biology, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Danish Headache Center and Danish Multiple Sclerosis Center, Copenhagen University Hospital, Rigshospitalet Glostrup, Glostrup, Denmark
| | - Tine Kirkeskov Lundquist
- Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
| | - Torben Hansen
- Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
| | - Torben Lykke Sørensen
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Clinical Eye Research Division, Department of Ophthalmology, Zealand University, Hospital, Roskilde, Denmark
| | - Torben Sigsgaard
- BERTHA Big Data Centre for Environment and Health, Aarhus University, Aarhus, Denmark
- Department of Public Health, Aarhus University, DK-8000, Aarhus, Denmark
| | - Kaspar René Nielsen
- Department of Clinical Immunology, Aalborg University Hospital, Aalborg, Denmark
| | - Mie Topholm Bruun
- Department of Clinical Immunology, Odense University Hospital, Odense, Denmark
| | - Henrik Hjalgrim
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark
- Danish Cancer Society Research Center, Danish Cancer Society, Copenhagen, Denmark
- Department of Hematology, Copenhagen University Hospital, Copenhagen, Denmark
| | | | - Klaus Rostgaard
- Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark
- Danish Cancer Society Research Center, Danish Cancer Society, Copenhagen, Denmark
| | - Erik Sørensen
- Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
| | - Ole Birger Pedersen
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Department of Clinical Immunology, Zealand University Hospital, Køge, Denmark
| | - Sisse Rye Ostrowski
- Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
| | - Christian Erikstrup
- Department of Clinical Immunology, Aarhus University Hospital, Aarhus, Denmark
- Department of Clinical Medicine, Aarhus University, Aarhus, Denmark
- BERTHA Big Data Centre for Environment and Health, Aarhus University, Aarhus, Denmark
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Grodin EN. Neuroimmune modulators as novel pharmacotherapies for substance use disorders. Brain Behav Immun Health 2024; 36:100744. [PMID: 38435721 PMCID: PMC10906159 DOI: 10.1016/j.bbih.2024.100744] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/20/2023] [Revised: 12/20/2023] [Accepted: 02/20/2024] [Indexed: 03/05/2024] Open
Abstract
One promising avenue of research is the use of neuroimmune modulators to treat substance use disorders (SUDs). Neuroimmune modulators target the interactions between the nervous system and immune system, which have been found to play a crucial role in the development and maintenance of SUDs. Multiple classes of substances produce alterations to neuroimmune signaling and peripheral immune function, including alcohol, opioids, and psychostimulants Preclinical studies have shown that neuroimmune modulators can reduce drug-seeking behavior and prevent relapse in animal models of SUDs. Additionally, early-phase clinical trials have demonstrated the safety and feasibility of using neuroimmune modulators as a treatment for SUDs in humans. These therapeutics can be used as stand-alone treatments or as adjunctive. This review summarizes the current state of the field and provides future directions with a specific focus on personalized medicine.
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Affiliation(s)
- Erica N. Grodin
- Department of Psychology, University of California at Los Angeles, Los Angeles, CA, USA
- Department of Psychiatry and Biobehavioral Sciences, University of California at Los Angeles, Los Angeles, CA, USA
- Cousins Center for Psychoneuroimmunology, University of California at Los Angeles, Los Angeles, CA, USA
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Mohamedi Y, Fontanil T, Vega JA, Cobo T, Cal S, Obaya ÁJ. Lung Inflammatory Phenotype in Mice Deficient in Fibulin-2 and ADAMTS-12. Int J Mol Sci 2024; 25:2024. [PMID: 38396702 PMCID: PMC10888546 DOI: 10.3390/ijms25042024] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/30/2023] [Revised: 01/23/2024] [Accepted: 01/29/2024] [Indexed: 02/25/2024] Open
Abstract
Interaction between extracellular matrix (ECM) components plays an important role in the regulation of cellular behavior and hence in tissue function. Consequently, characterization of new interactions within ECM opens the possibility of studying not only the functional but also the pathological consequences derived from those interactions. We have previously described the interaction between fibulin2 and ADAMTS-12 in vitro and the effects of that interaction using cellular models of cancer. Now, we generate a mouse deficient in both ECM components and evaluate functional consequences of their absence using different cancer and inflammation murine models. The main findings indicate that mice deficient in both fibulin2 and ADAMTS12 markedly increase the development of lung tumors following intraperitoneal urethane injections. Moreover, inflammatory phenotype is exacerbated in the lung after LPS treatment as can be inferred from the accumulation of active immune cells in lung parenchyma. Overall, our results suggest that protective effects in cancer or inflammation shown by fibulin2 and ADAMTS12 as interactive partners in vitro are also shown in a more realistic in vivo context.
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Affiliation(s)
- Yamina Mohamedi
- Departamento de Bioquímica y Biología Molecular, Universidad de Oviedo, 33006 Oviedo, Spain
| | - Tania Fontanil
- Departamento de Bioquímica y Biología Molecular, Universidad de Oviedo, 33006 Oviedo, Spain
| | - José A. Vega
- Departamento de Morfología y Biología Celular, Universidad de Oviedo, 33006 Oviedo, Spain
- Facultad de Ciencias de la Salud, Universidad Autónoma de Chile, Providencia—Área Metropolinana, Santiago de Chile 7500912, Chile
| | - Teresa Cobo
- Departamento de Cirugía y Especialidades Médico-Quirúrgicas, Universidad de Oviedo, 33006 Oviedo, Spain
- Instituto Asturiano de Odontología (IAO), 33006 Oviedo, Spain
| | - Santiago Cal
- Departamento de Bioquímica y Biología Molecular, Universidad de Oviedo, 33006 Oviedo, Spain
| | - Álvaro J. Obaya
- Departamento de Biología Funcional, Área de Fisiología, Universidad de Oviedo, 33006 Oviedo, Spain
- Instituto Universitario de Oncología del Principado de Asturias (IUOPA), 33006 Oviedo, Spain
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Sethi S, Shahin A, Rahim INA. Association of Human Papillomavirus Infection with Tonsillar Cancers: A Systematic Review. Indian J Otolaryngol Head Neck Surg 2024; 76:268-276. [PMID: 38440648 PMCID: PMC10908725 DOI: 10.1007/s12070-023-04140-2] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/13/2023] [Accepted: 08/11/2023] [Indexed: 03/06/2024] Open
Abstract
Vaccinations have shown a decrease in human papillomavirus (HPV) infection-related cervical cancer in women, but there has been a sharp rise in the HPV infection-related oropharyngeal cancer cases over the past few decades. Recent studies have suggested the association of HPV infections with tonsillar cancers as well and suggestions regarding preventive tonsillectomies in order to achieve a decrease in HPV infection-related oropharyngeal or tonsillar cancer have arisen. However, there is limited cumulative evidence validated at a global level to support the endorsement of this strategy. This research revolves around the concept of burden of tonsillar carcinomas due to oropharyngeal HPV infection. Thus, a systematic review and meta-analysis of existing studies was undertaken to estimate the pooled prevalence of tonsillar cancer associated with oropharyngeal HPV infection. Published articles on tonsillar cancer with and without HPV infection from PubMed, Embase, Scopus and Web of Science were systematically searched from inception until 23 December 2021. A random-effects model was used to estimate the pooled prevalence forest plots. The systematic review revealed that 50% of the reported cases of tonsillar cancer had an oropharyngeal HPV infection, questioning the preventive nature of an early tonsillectomy which is essentially an invasive surgical procedure. Large heterogeneity was reported in the included studies, and there was insufficient data for sub-group analysis. Future research and representative studies are required to thoroughly explore the correlation between HPV infection and tonsillar cancer. Supplementary Information The online version contains supplementary material available at 10.1007/s12070-023-04140-2.
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Affiliation(s)
- Sneha Sethi
- Australian Research Center for Population Oral Health, Adelaide Dental School, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, SA 5000 Australia
| | - Alana Shahin
- Adelaide Medical School, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, SA Australia
| | - Intisar Nuha Abd Rahim
- Adelaide Medical School, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, SA Australia
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Mahabee-Gittens EM, Matt GE, Mazzella MJ, Doucette JT, Ratnani P, Merianos AL. Inflammatory marker levels in children with tobacco smoke exposure. Cytokine 2024; 173:156448. [PMID: 37980882 PMCID: PMC10843711 DOI: 10.1016/j.cyto.2023.156448] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/08/2023] [Revised: 11/12/2023] [Accepted: 11/14/2023] [Indexed: 11/21/2023]
Abstract
BACKGROUND Tobacco smoke exposure (TSE) has inflammatory and immunosuppressive effects which may be associated with altered levels of inflammatory markers and pediatric illnesses. OBJECTIVE The primary objective was to examine the associations of cotinine-confirmed and parent-reported child TSE patterns and discharge diagnoses with C-reactive protein (CRP), IL-8, and IL-10 in 0-11-year-old pediatric emergency department (PED) patients who lived with ≥ 1 smoker. METHODS Saliva samples were obtained from 115 children with a mean (SD) age of 3.5 (3.1) years during the PED visit (T0). Saliva was analyzed for cotinine, CRP, IL-8, and IL-10. Parents self-reported their children's TSE patterns; children's medical records were reviewed to identify and categorize discharge diagnoses. Linear regression models were utilized to find T0 associations of cotinine-confirmed and parent-reported child TSE patterns, and PED diagnoses with each inflammatory marker. All models were adjusted for child race/ethnicity, child sex, annual household income, and housing type. The TSE models also adjusted for child discharge diagnosis. RESULTS At T0, the geometric mean (GeoM) of cotinine was 4.1 ng/ml [95 %CI = 3.2-5.2]; the GeoMs of CRP, IL-8, and IL-10 were 3,326 pg/ml [95 %CI = 2,696-4,105], 474 pg/ml [95 %CI = 386-583], and 1.1 pg/ml [95 %CI = 0.9-1.3], respectively. Parent-reported child TSE patterns were positively associated with ln-transformed CRP levels, while adjusting for the covariates (β^ = 0.012 [95 %CI:0.004-0.020], p = 0.037). In the parent-reported child TSE pattern model, there were significant positive associations between the covariate of child age with CRP and IL-8 levels (p = 0.028 and p < 0.001, respectively). Children with a bacterial diagnosis had higher IL-8 levels (p = 0.002) compared to the other diagnosis groups. CONCLUSIONS Results indicate that parent-reported child TSE increases the expression of CRP in ill children and supports prior work demonstrating that IL-8 is higher in children with TSE who have bacterial infections. These findings should be examined in future research with ill children with and without TSE.
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Affiliation(s)
- E Melinda Mahabee-Gittens
- Division of Emergency Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
| | - Georg E Matt
- Department of Psychology, San Diego State University, San Diego, CA, USA
| | - Matthew J Mazzella
- Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA
| | - John T Doucette
- Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA
| | - Parita Ratnani
- Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA
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Xu J, Liu W, Liu X, Zhou X, Li G. Alcohol drinking, smoking, and cutaneous melanoma risk: Mendelian randomization analysis. GACETA SANITARIA 2023; 37:102351. [PMID: 38052122 DOI: 10.1016/j.gaceta.2023.102351] [Citation(s) in RCA: 8] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 07/13/2023] [Revised: 10/26/2023] [Accepted: 11/06/2023] [Indexed: 12/07/2023]
Abstract
OBJECTIVE To investigate the causal relationship between poor lifestyle habits, such as smoking and drinking, and cutaneous malignant melanoma. METHOD In the present study, alcohol consumption and smoking were used as exposure factors, and single nucleotide polymorphisms closely associated with alcohol consumption and smoking were used as instrumental variables, while cutaneous melanoma was set as an outcome variable. Two-sample Mendelian randomization analyses were run between alcohol consumption and melanoma and smoking and melanoma to investigate their causal associations, respectively. RESULTS We found a positive and statistically significant causal effect of alcohol intake on the risk of cutaneous malignant melanoma (OR: 2.23; 95%CI: 1.11-4.47; p=0.02). The present study showed no significant causal relationship between cigarettes per day and cutaneous melanoma (OR: 0.85; 95%CI: 0.54-1.35; p=0.50) or smoking initiation and cutaneous melanoma (OR: 1.02; 95%CI: 0.74-1.39; p=0.88). CONCLUSIONS This study provides Mendelian randomization evidence supporting alcohol consumption as a risk factor for cutaneous malignant melanoma. And the causal relationship between smoking and cutaneous malignant melanoma still needs to be further investigated.
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Affiliation(s)
- Jiaxiang Xu
- The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China
| | - Wenhui Liu
- The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China
| | - Xuanjun Liu
- The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China
| | - Xinlong Zhou
- The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China
| | - Guangshuai Li
- The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.
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Wang Z, Zhang M. Smoking and the risk of atopic dermatitis: A two-sample mendelian randomization study. Medicine (Baltimore) 2023; 102:e36050. [PMID: 37960725 PMCID: PMC10637425 DOI: 10.1097/md.0000000000036050] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/15/2023] [Accepted: 10/19/2023] [Indexed: 11/15/2023] Open
Abstract
Atopic dermatitis (AD) is considered to be one of the most common chronic diseases. It has been shown that smoking is associated with atopic dermatitis, but previous studies were mainly observational, which may be biased. The present study conducted a 2-sample mendelian randomization (MR) study to investigate the causal relationship. The present study obtained data on "ever smoked" and "atopic dermatitis" from published large-scale genome-wide association studies. The data were obtained from the UK Biobank and BioBank Japan. Three methods were used to perform a 2-sample MR analysis and also performed sensitivity analysis. The odds ratio and 95% confidence interval (CI) between smoking and AD calculated by MR-Egger regression, weighted median, and random-effects inverse variance weighting method were 1.096 (95% CI.756-1.587) and 1.159 (95% CI 1.040-1.292), respectively, 1.137 (95% CI .975-1.325). The inverse variance weighting method showed statistical significance between the 2 and a causal relationship between smoking and AD. In conclusion, the results of our MR analysis suggest that smoking is likely to affect the incidence of AD.
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Affiliation(s)
- Zhenni Wang
- Department of Dermatology, Chaohu Hospital of Anhui Medical University, Anhui, China
| | - Minghai Zhang
- Department of Dermatology, Chaohu Hospital of Anhui Medical University, Anhui, China
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Malevolti MC, Maci C, Lugo A, Possenti I, Gallus S, Gorini G, Carreras G. Second-hand smoke exposure and cervical cancer: a systematic review and meta-analysis. J Cancer Res Clin Oncol 2023; 149:14353-14363. [PMID: 37516982 DOI: 10.1007/s00432-023-04841-9] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/06/2023] [Accepted: 05/04/2023] [Indexed: 08/01/2023]
Abstract
PURPOSE The association between second-hand smoke (SHS) exposure and cervical cancer (CC) risk is still unclear. The aim of this study is to provide an accurate and updated estimate of this association. METHODS Through an original methodology to identify original publications, we conducted a systematic review and meta-analysis of all epidemiological studies published up to October 2022 evaluating the association between SHS exposure and CC risk among female non-smokers. Meta-analytic estimates were obtained using random-effects models and dose-response relationships were derived using log-linear functions. RESULTS Out of 25 eligible studies, 21 were included in the meta-analysis, providing a pooled relative risk (RR) of cervical intraepithelial neoplasia (CIN) of grade 2 or higher of 1.52 (95% confidence interval, CI 1.30-1.78, 21 studies) for overall SHS exposure versus non-exposure. When restricting the analysis to invasive CC, the pooled RR was 1.42 (95% CI 1.17-1.71, 13 studies), whereas the pooled RR for CIN was 1.50 (95% CI 1.22-1.84, 6 studies). Analyzing RR by setting or source of SHS exposure resulted in significant associations with CC risk for SHS exposure at home (RR for CIN2+ 1.49, 95% CI 1.21-1.84, 14 studies), in non-specified settings (RR for CIN2+ 1.64, 95% CI 1.20-2.23, 8 studies) and from partner (RR for CIN2+ 1.55, 95% CI 1.25-1.94, 10 studies). The risk of CIN2+ significantly increased linearly with the intensity and pack-years of SHS exposure. CONCLUSION This comprehensive review and meta-analysis confirmed the association of SHS exposure with CC, further suggesting the need to raise concern about SHS exposure in the population.
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Affiliation(s)
- Maria Chiara Malevolti
- Oncologic Network, Prevention and Research Institute (ISPRO), Via Cosimo il Vecchio 2, 50139, Florence, Italy
| | - Caterina Maci
- Oncologic Network, Prevention and Research Institute (ISPRO), Via Cosimo il Vecchio 2, 50139, Florence, Italy
| | - Alessandra Lugo
- Department of Medical Epidemiology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy
| | - Irene Possenti
- Department of Medical Epidemiology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy
| | - Silvano Gallus
- Department of Medical Epidemiology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy
| | - Giuseppe Gorini
- Oncologic Network, Prevention and Research Institute (ISPRO), Via Cosimo il Vecchio 2, 50139, Florence, Italy
| | - Giulia Carreras
- Oncologic Network, Prevention and Research Institute (ISPRO), Via Cosimo il Vecchio 2, 50139, Florence, Italy.
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Hussain N, Ikram N, Khan KUR, Hussain L, Alqahtani AM, Alqahtani T, Hussain M, Suliman M, Alshahrani MY, Sitohy B. Cichorium intybus L. significantly alleviates cigarette smoke-induced acute lung injury by lowering NF-κB pathway activation and inflammatory mediators. Heliyon 2023; 9:e22055. [PMID: 38045213 PMCID: PMC10692792 DOI: 10.1016/j.heliyon.2023.e22055] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/06/2023] [Revised: 11/02/2023] [Accepted: 11/02/2023] [Indexed: 12/05/2023] Open
Abstract
Background Cigarette smoke (CS) is one of the primary causes of acute lung injury (ALI) via provoking pulmonary inflammation and oxidative stress. Despite substantial studies, no effective treatment for ALI is presently available. Purpose New prospective treatment options for ALI are required. Thus, this project was designed to investigate the in vivo and in vitro protective effects of 70 % methanolic-aqueous crude extract of whole plant of Cichorium intybus (Ci.Mce) against CS-induced ALI. Study design /methods: Initially, male Swiss albino mice were subjected to whole-body CS exposure for 10 continuous days to prepare CS-induced ALI models. Normal saline (10 mL/kg), Ci.Mce (100, 200, 300 mg/kg), and Dexamethasone (1 mg/kg) were orally administered to respective animal groups 1 h prior to CS-exposure. 24 hrs after the last CS-exposure, BALF and lungs were harvested to study the key characteristics of ALI. Next, HPLC analysis was done to explore the phytoconstituents. Results Ci.Mce exhibited significant reductions in lung macrophage and neutrophil infiltration, lung weight coefficient, and albumin exudation. Additionally, it effectively ameliorated lung histopathological alterations and hypoxemia. Notably, Ci.Mce exerted inhibitory effects on the excessive generation of IL-6, IL-1β, and KC in both CS-induced ALI murine models and CSE-stimulated RAW 264.7 macrophages. Noteworthy benefits included the attenuation of oxidative stress induced by CS, evidenced by decreased levels of MDA, TOS, and MPO, alongside enhanced TAC production. Furthermore, Ci.Mce demonstrated a marked reduction in CS-induced NF-κB expression, both in vivo and in vitro. Conclusion Consequently, Cichorium intybus could be a therapeutic option for CS-induced ALI due to its ability to suppress inflammatory reactions, mitigate oxidative stress, and quell NF-κB p65 activation.
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Affiliation(s)
- Nadia Hussain
- Department of Pharmaceutical Sciences, College of Pharmacy, Al Ain University, Al Ain, 64141, United Arab Emirates
| | - Nadia Ikram
- Faculty of Pharmacy, The Islamia University of Bahawalpur, Bahawalpur, 63100, Pakistan
| | - Kashif ur Rehman Khan
- Faculty of Pharmacy, The Islamia University of Bahawalpur, Bahawalpur, 63100, Pakistan
| | - Liaqat Hussain
- Department of Pharmacology, Government College University, Faisalabad, 38,000, Pakistan
| | - Ali M. Alqahtani
- Department of Pharmacology, College of Pharmacy, King Khalid University, Abha, 62529, Saudi Arabia
| | - Taha Alqahtani
- Department of Pharmacology, College of Pharmacy, King Khalid University, Abha, 62529, Saudi Arabia
| | - Musaddique Hussain
- Faculty of Pharmacy, The Islamia University of Bahawalpur, Bahawalpur, 63100, Pakistan
| | - Muath Suliman
- Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Khalid University, P.O. Box 61413, Abha, 9088, Saudi Arabia
| | - Mohammad Y. Alshahrani
- Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Khalid University, P.O. Box 61413, Abha, 9088, Saudi Arabia
| | - Basel Sitohy
- Department of Clinical Microbiology, Infection and Immunology, Umeå University, SE-90185, Umeå, Sweden
- Department of Radiation Sciences, Oncology, Umeå University, SE-90185, Umeå, Sweden
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Maisha JA, El-Gabalawy HS, O’Neil LJ. Modifiable risk factors linked to the development of rheumatoid arthritis: evidence, immunological mechanisms and prevention. Front Immunol 2023; 14:1221125. [PMID: 37767100 PMCID: PMC10520718 DOI: 10.3389/fimmu.2023.1221125] [Citation(s) in RCA: 17] [Impact Index Per Article: 8.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/11/2023] [Accepted: 08/24/2023] [Indexed: 09/29/2023] Open
Abstract
Rheumatoid Arthritis (RA) is a common autoimmune disease that targets the synovial joints leading to arthritis. Although the etiology of RA remains largely unknown, it is clear that numerous modifiable risk factors confer increased risk to developing RA. Of these risk factors, cigarette smoking, nutrition, obesity, occupational exposures and periodontal disease all incrementally increase RA risk. However, the precise immunological mechanisms by which these risk factors lead to RA are not well understood. Basic and translational studies have provided key insights into the relationship between inflammation, antibody production and the influence in other key cellular events such as T cell polarization in RA risk. Improving our general understanding of the mechanisms which lead to RA will help identify targets for prevention trials, which are underway in at-risk populations. Herein, we review the modifiable risk factors that are linked to RA development and describe immune mechanisms that may be involved. We highlight the few studies that have sought to understand if modification of these risk factors reduces RA risk. Finally, we speculate that modification of risk factors may be an appealing avenue for prevention for some at-risk individuals, specifically those who prefer lifestyle interventions due to safety and economic reasons.
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Affiliation(s)
| | | | - Liam J. O’Neil
- Manitoba Centre for Proteomics and Systems Biology, Department of Internal Medicine, University of Manitoba, Winnipeg, MB, Canada
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Lin C, Lin L, Chen T, Ye Y, Chiang B. The expression of nicotinic acetylcholine receptor subunits and their associations with local immune cells and prognosis in oral squamous cell carcinoma. Cancer Med 2023; 12:18918-18930. [PMID: 37654227 PMCID: PMC10557882 DOI: 10.1002/cam4.6482] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/26/2023] [Revised: 07/16/2023] [Accepted: 08/17/2023] [Indexed: 09/02/2023] Open
Abstract
BACKGROUND Nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels that may be responsible for cancer cell proliferation, epithelial-mesenchymal transition (EMT), and immune regulation. However, little is known about the associations of different nAChR subunits with tumor microenvironment in oral squamous cell carcinoma (OSCC). METHODS We retrospectively reviewed pathology samples from 75 OSCC patients by immunohistochemistry. In addition, a cohort of 307 OSCC patients in The Cancer Genome Atlas was analyzed. RESULTS Subunit α1 was specific to peri-OSCC skeletal muscle. Increased α1 was associated with increased CD44 (cancer stem cells), increased CD3 and 8 (T cells), increased CD56 and 16 (natural killer cells), a decreased T stage, and an increased N stage. Increased α3 was associated with increased CD56 and 16. Increased α5 was associated with decreased CD3, 8, and 56, a decreased T stage, an increased N stage, worse survival, and decreased epithelial features. Increased α7 was associated with increased CD3, 8, 56, and 16, decreased tumor/peritumor ratios of CD3, 8, and 56 immune cells, and increased epithelial features. Increased local immune cells were associated with a better prognosis. CONCLUSIONS α5 is the only subunit associated with decreased local immune cells and worse survival, while α1, α3, and α7 are associated with increased local immune cells in OSCC. α5 and α7 are correlated with different EMT states to be mesenchymal-like and epithelial-like OSCC, respectively. Protein expression data of the nAChR subunits, complementary to gene expression data, could provide meaningful information regarding the EMT status of OSCC associated with immune responses and prognosis.
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Affiliation(s)
- Chi‐Maw Lin
- Department of OtolaryngologyNational Taiwan University Hospital, Yun‐Lin BranchTaipeiTaiwan
- Graduate Institute of Clinical Medicine, College of MedicineNational Taiwan UniversityTaipeiTaiwan
| | - Long‐Wei Lin
- Department of PathologyNational Taiwan University Hospital, Yun‐Lin BranchTaipeiTaiwan
| | - Tseng‐Cheng Chen
- Department of OtolaryngologyNational Taiwan University Hospital and National Taiwan University, College of MedicineTaipeiTaiwan
| | - Yi‐Ling Ye
- Department of BiotechnologyNational Formosa UniversityHuweiTaiwan
| | - Bor‐Luen Chiang
- Graduate Institute of Clinical Medicine, College of MedicineNational Taiwan UniversityTaipeiTaiwan
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