The global incidence of colorectal cancer (CRC) is increasing. In the majority of CRC cases, colon cancer develops from alterations in the adenoma-carcinoma sequence pathway. Currently, there are few studies regarding the effects of enteric viruses on the adenoma-carcinoma sequence pathway, and subsequently, the progression and development of the CRC. Here, fecal and tissue samples from a normal control group, an adenomatous polyp group, and a colorectal adenocarcinoma group were collected to gain a deeper understanding of the variations in enteric viruses in CRC patients and to analyze their significance. With the progression of CRC from adenoma to adenocarcinoma, the number of DNA viruses in the virus-like particles (VLPs) of fecal and tissue samples gradually increased, and there were distinct differences in the composition of enteric viruses among the different groups. Multiple species correlation analysis revealed extensive interactions among viruses, bacteria, and fungi in fecal and tissue samples. Functional analysis also revealed that the functional pathways in fecal and tissue samples also underwent significant changes. In conclusion, the changes in the composition and function of enteric viruses in the progression of CRC via adenoma-carcinoma sequence pathway were analyzed in this study, and these changes hold certain importance for exploring the role of enteric viruses in the occurrence of this disease; however, their mode of action and specific mechanisms require further investigation.

Background/Objectives: The aim of this study was to qualitatively and quantitatively assess the bacterial domain of the gut microbiome in elderly patients with type 2 diabetes (T2D), with a focus on sex differences, glycemic control, and lipid disorders. Methods: This study included 60 older adults with T2D (38 women and 22 men) treated with metformin or a combination of metformin and insulin. The gut microbiota was profiled using 16S rRNA gene sequencing. Statistical analyses, including correlation analysis and multiple regression, were performed to identify the associations between microbial taxa, sex, and metabolic parameters. Results: No statistically significant differences in alpha or beta diversity were observed between the sexes. Multiple regression analysis indicated a positive relationship between Tenericutes and HbA1c in male participants (β = 2.22931, CI [0.75, 3.70], R = 0.67; R2 = 0.36; unadjusted p = 0.0052; adjusted p = 0.0496). In female participants, G0' (β = -2.24107, CI [-3.19, -1.30], R = 0.78; R2 = 0.58; unadjusted p = 0.00003; adjusted p = 0.0005) and HbA1c (β = -1.86670, CI [-2.61, -1.12], R = 0.78; R2 = 0.58; unadjusted p = 0.00001; adjusted p = 0.0003) correlated negatively with Verrucomicrobia as well G0' (β = -1.90427, CI [-2.95, -0.85], R = 0.46; R2 = 0.17; unadjusted p = 0.0008; adjusted p = 0.007) and HbA1c (β = -1.69561, CI [-2.52, -0.87], R = 0.46; R2 = 0.17; unadjusted p = 0.0002; adjusted p = 0.002) correlated negatively with OD1 bacteria, known as Parcubacteria. Conclusions: In this elderly population with type 2 diabetes, biological sex did not significantly affect the gut microbiota diversity. However, several exploratory associations between microbial taxa and metabolic parameters differed between men and women, suggesting that sex may influence specific aspects of microbiota-metabolism interactions. These preliminary findings underscore the importance of considering both age- and sex-related factors when investigating the gut microbiome in the context of type 2 diabetes.

Bacterial detection is pivotal for the timely diagnosis and effective treatment of infectious diseases. Microfluidic platforms offer advantages over traditional methods, including heightened sensitivity, rapid analysis, and minimal sample volume requirements. Traditional clinical methods for bacterial identification often involve extended processing times and necessitate high pathogen concentrations, resulting in delayed diagnoses and missed treatment opportunities. Microfluidic technology overcomes these limitations by facilitating rapid bacterial identification at lower biomass levels, thus ensuring prompt and precise treatment interventions. Additionally, bacteria-driven inflammation has been associated with the development and progression of various diseases, including cancer. Elucidating the complex interplay between bacteria, inflammation, and disease is essential for devising effective disease models and therapeutic strategies. Microfluidic platforms have been used to construct in vitro disease models that accurately replicate the intricate microenvironment that bacteria-driven inflammation affects. These models offer valuable insights into bacteria-driven inflammation and its impact on disease progression, such as cancer metastasis and therapeutic responses. This review examines recent advancements in bacterial detection using microfluidics and assesses the potential of this technology as a robust tool for exploring bacteria-driven inflammation in the context of cancer.

Metabolic diseases, such as obesity, type 2 diabetes, and non-alcoholic fatty liver disease, have emerged as major global health challenges. Recent research has revealed that the gut microbiome is closely associated with the development of these conditions. The Food and Drug Administration has recognized certain probiotic strains with therapeutic potential, classifying them as live biotherapeutic products (LBPs). LBPs, which are derived from naturally occurring microorganisms, may present an effective strategy for treating metabolic diseases by restoring gut microbiota balance and regulating metabolic functions. This review explores the development of LBPs specifically for metabolic disease treatments, covering every phase from strain identification, non-clinical and clinical trials, manufacturing and formulation to regulatory approval. Furthermore, it addresses the challenges involved in the commercialization of these therapies. By offering critical insights into the research and development of LBPs for metabolic disease treatment, this review aims to contribute to the progress of these promising therapies.

The appearance of cancer progresses through a multistep process that includes genetic, epigenetic, mutational, inflammatory and metabolic disturbances to signaling pathways within an organ. The combined influence of these changes will dictate the growth properties of the cells; the direction of further malignancy depends on the severity of these "disturbances". The molecular mechanisms driving abnormal inflammation and metabolism are beginning to be identified and, in some cases, are quite prominent in pre-condition states of cancer and are significant drivers of the malignant phenotype. As such, utilizing signaling pathways linked to inflammation and metabolism as biomarkers of cancer is an emerging method and includes pathways beyond those well characterized to drive metabolism or inflammation. In this review, we will discuss several emerging elements influencing proliferation, inflammation and metabolism that may play a part as drivers of the cancer phenotype. These include AMPK and leptin (linked to metabolism), NOD2/RIPK2, TAK1 (linked to inflammation), lactate and pyruvate transporters (monocarboxylate transporter [MCT], linked to mitochondrial biogenesis and metabolism) and RASSF1A (linked to proliferation, cell death, cell cycle control, inflammation and epigenetics). We speculate that the aforementioned elements are important drivers of carcinogenesis that should be collectively referenced as being involved in "ImmunoMET Oncogenesis", a new tripartite description of the role of elements in driving cancer. This term would suggest that for a better understanding of cancer, we need to understand how proliferation, inflammation and metabolic pathways are impacted and how they influence classical drivers of malignant transformation in order to drive ImmunoMET oncogenesis and the malignant state.

Obesity is a growing health concern worldwide, including United Arab Emirates. Bariatric surgery is an effective treatment option, with to date unclear weight loss mechanisms. In this prospective study, we explored post-bariatric surgery changes in energy homeostasis, gut peptides, hormones, and gut microbiota.

We recruited 19 Emirati adults who were planning to undergo sleeve gastrectomy (SG). We assessed the energy requirements using 24-hour diet recalls, indirect calorimetry for resting energy expenditure (REE), and a questionnaire for appetite. Anthropometrics included body mass index (BMI), waist circumference, waist-to-height ratio, fat mass, fat-free mass, and percentage of body fat. Gut peptides, including peptide YY (PYY), glucagon-like peptide-1/2 (GLP-1/2), ghrelin (GHR), cholecystokinin (CCK), insulin, and leptin, were quantified using ELISA. Gut microbiota composition at phylum and genus levels, including the Firmicutes/Bacteroidetes (F/B) ratio and alpha (α) and beta (β) diversity, was determined by sequencing amplicons of the V3-V4 region of the 16S rRNA at baseline and three months post-surgery. Comparisons used paired sample T-test, Wilcoxon, and McNemar test. QIIME 2 was used to identify taxa and their relative abundance; subsequent analyses were done in R for (α) and (β) diversity (package qiime2R) and Wilcoxon signed-rank test in R for differences in microbiota at phylum and genus levels. We conducted Spearman correlation analyses between genera and energy homeostasis, appetite, anthropometrics, hormones, and gut peptides.

At three months post-SG, energy intake, appetite, all anthropometric indices, insulin, leptin, and GLP-1 significantly decreased; PYY and GHR significantly increased, and REE was stable. β-diversity of the gut microbiota and its composition at phylum and genus levels significantly changed post-surgery, yet F/B remained constant. Energy intake, BMI, and appetite negatively correlated with several taxa that significantly increased post-SG.

Gut peptides, hormones, and microbiota change partly account for bariatric surgery's weight-loss benefits. Understanding these alterations can inform personalized interventions targeting obesity.

Metabolism is at the core of all functions of living cells as it provides Gibbs free energy and building blocks for synthesis of macromolecules, which are necessary for structures, growth, and proliferation. Metabolism is a complex network composed of thousands of reactions catalyzed by enzymes involving many co-factors and metabolites. Traditionally it has been difficult to study metabolism as a whole network and most traditional efforts were therefore focused on specific metabolic pathways, enzymes, and metabolites. By using engineering principles of mathematical modeling to analyze and study metabolism, as well as engineer it, that is, design and build, new metabolic features, it is possible to gain many new fundamental insights as well as applications in biotechnology. Here, we present the history and basic principles of engineering metabolism, as well as the newest developments in the field. We are using examples of applications in: (1) production of protein pharmaceuticals and chemicals; (2) basic studies of metabolism; and (3) impacting health care. We will end by discussing how engineering metabolism can benefit from advances in artificial intelligence (AI)-based models.

Previous researches have suggested an important association between gut microbiota (GM) and vascular pathologies such as atherosclerosis. This study aimed to explore the association between 196 GM taxa and retinal vein occlusion (RVO).

This study used Mendelian randomization (MR), linkage disequilibrium score regression (LDSC), and polygenic overlap analysis. Genome-wide association study (GWAS) data associated with 196 GM taxa was obtained from the MiBioGen consortium, involving a large number of European-ancestry participants. GWAS data of RVO was obtained from the FinnGen consortium and another study that also involved European-ancestry participants. Inverse-variance weighted was used as the primary approach for MR estimation. Moreover, LDSC and polygenic overlap analyses were performed to evaluate the genetic correlation between GM taxa and RVO.

The MR results identified the association of six GM taxa, including class Bacilli, order Lactobacillales, family Streptococcaceae, genus Clostridium innocuum group, genus Family XIII AD3011 group, and genus Subdoligranulum with the development of RVO. In addition, the polygenic overlap analysis supported the genetic association between GM and RVO.

Our findings confirmed the association between six GM taxa and the development of RVO, thereby highlighting the effects of GM on retinal vascular health.

The results may provide the rationale for developing GM-based strategies for preventing the onset of RVO.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent metabolic disorder characterized by hepatic steatosis associated with metabolic abnormalities. Recent research has shed light on the intricate interplay among interleukin-1 receptor 1 (IL1R1), gut microbiota, and bile acids in the pathogenesis of MASLD. This review aims to provide a comprehensive overview of the current understanding of the role of IL1R1, gut microbiota, and bile acids in MASLD, exploring their interrelationships and potential mechanisms. We summarize the evidence supporting the involvement of IL1R1 in inflammation, discuss the influence of gut microbiota on bile acid metabolism and its influence on liver health, and elucidate the bidirectional interactions among IL1R1 signaling, gut microbiota composition, and bile acid homeostasis in MASLD. Furthermore, we highlight emerging therapeutic strategies targeting these interrelated pathways for the management of MASLD.

Diet significantly influences the human gut microbiota, a key player in health. We analyzed shotgun metagenomic sequencing data from healthy individuals with long-term dietary patterns-vegan, flexitarian, or omnivore-and included detailed dietary surveys and blood biomarkers. Dietary patterns notably affected the bacterial community composition by altering the relative abundances of certain species but had a minimal impact on microbial functional repertoires. However, diet influenced microbial functionality at the strain level, with diet type linked to strain genetic variations. We also found molecular signatures of selective pressure in species enriched by specific diets. Notably, species enriched in omnivores exhibited stronger positive selection, such as multiple iron-regulating genes in the meat-favoring bacterium Odoribacter splanchnicus, an effect that was also validated in independent cohorts. Our findings offer insights into how diet shapes species and genetic diversity in the human gut microbiota.

Understanding the relationship between dietary fat and physiological responses is crucial in species adapted to arid environments where water scarcity is common. In this study, we present a comprehensive exploration of gene expression across five tissues (kidney, liver, lung, gastrointestinal tract and hypothalamus) and 17 phenotypic measurements, investigating the effects of dietary fat in the desert-adapted cactus mouse (Peromyscus eremicus). We show impacts on immune function, circadian gene regulation and mitochondrial function for mice fed a lower-fat diet compared with mice fed a higher-fat diet. In arid environments with severe water scarcity, even subtle changes in organismal health and water balance can affect physical performance, potentially impacting survival and reproductive success. This study sheds light on the complex interplay between diet, physiological processes and environmental adaptation, providing valuable insights into the multifaceted impacts of dietary choices on organismal well-being and adaptation strategies in arid habitats.

Dysfunction in the prefrontal cortex can lead to cognitive inflexibility due to multifactorial causes as included cardiometabolic disorders, stress, inadequate diets, as well as an imbalance of the gut-brain axis microbiota. However, these risk factors have not been evaluated jointly. The purpose of this study was to evaluate the effect of physical stress (MS: Male Stress and FS: Female Stress) and high-fat diet (MD: Male Diet and FD: Female Diet) supplementation on the gut microbiota and cognitive flexibility.

The study was performed on 47 mice, 30 male (M) and 17 female (F) BALBc, exposed to chronic stress physical (S) and high-fat diet (D). Cognitive flexibility was evaluated using the Attentional Set-Shifting Test (ASST) and the gut microbiota composition in terms of relative abundance (%) and alpha-beta diversity.

Results showed that S and D reduced cognitive flexibility in male and female mice (p < 0.0001). Significant changes occurred in Alistipes spp. (MM vs. MS:MD; p < 0.0001), Barnesiella spp. (FC vs. FS; p = 0.0002; FC vs. FD, p = 0.0033); Dorea spp. (MC vs. MD, p = 0.0008; MM vs. MD, p < 0.0001) and Lactobacillus spp. (MC vs. MD and FM vs. FS, p < 0.0001; FM vs. MD, p = 0.0393) genera among groups. Predictive functional analysis (QIIME2 and PICRUSt2) showed a significant increase in the expression of histidine kinase, alanine dehydrogenase, glutamine synthase, glutamate synthase, arginine succinyl synthase, and tryptophan synthase genes (p < 0.05), the latter being a precursor of serotonin (5-HT).

Chronic physical stress and a high-fat diet modify cognitive flexibility and the composition and predictive function of the gut microbiota.

Correction of decreased diversity of the gut microbiome, which is characteristic of menopause, by supplementation with a synbiotic may attenuate or prevent dysbiosis processes and preserve bone mass. We describe the rationale and design of the OsteoPreP trial aimed at evaluating the effects of 12 months of supplementation with a synbiotic on bone and metabolic health in postmenopausal Caucasian women.

This is a randomized, double-blinded, placebo-controlled trial among 160 Caucasian, postmenopausal women with no current diagnosis of osteoporosis or supplementation with pro- or prebiotics, and no medical treatment affecting bone turnover. Dual-energy X-ray absorptiometry scans will be conducted at screening to confirm absence of osteoporosis. The primary outcome is the relative change (%) in total bone mineral density of the distal tibia at 12 months post-treatment between the active and placebo groups, as determined via high-resolution peripheral quantitative computed tomography. Secondary outcomes are the effects on immune system modulation and cognition, gut microbiota composition, and musculoskeletal and metabolic functions, with particular emphasis on blood glucose regulation.

The trial will inform on the efficacy and safety of a synbiotic containing both aerobic and anerobic bacterial strains and a prebiotic fiber on reduction in bone loss and on indices of blood glucose regulation. This trial may pave the way for an exciting field of translational research and be the underpinnings of the prevention strategy of osteoporosis and the management of metabolic dysfunction in postmenopausal women. The trial is registered with clinicaltrials.gov (NCT05348694).

Glaucoma is the primary cause of irreversible blindness globally. Different glaucoma subtypes are identified by their underlying mechanisms, and treatment options differ by its pathogenesis. Current management includes topical medications to lower intraocular pressure and surgical procedures like trabeculoplasty and glaucoma drainage implants. Fecal microbiota transplantation (FMT) is an almost effective and safe treatment option for recurrent Clostridium difficile infection. The relationship between bacterial populations, metabolites, and inflammatory pathways in retinal diseases indicates possible therapeutic strategies. Thus, incorporating host microbiota-based therapies could offer an additional treatment option for glaucoma patients. Here, we propose that combining FMT with standard glaucoma treatments may benefit those affected by this condition. Also, the potential safety, efficacy, cost-effectiveness and clinical applications are discussed.

Polycystic Ovary Syndrome (PCOS) is a metabolic disorder characterized by hyperandrogenism and related symptoms in women of reproductive age. Emerging evidence suggests that chronic low-grade inflammation plays a significant role in the development of PCOS. The gut microbiota, a complex bacterial ecosystem, has been extensively studied for various diseases, including PCOS, while the underlying mechanisms are not fully understood. This review comprehensively summarizes the changes in gut microbiota and metabolites observed in PCOS and their potential association with the condition. Additionally, we discuss the role of abnormal nuclear factor κB signaling in the pathogenesis of PCOS. These findings offer valuable insights into the mechanisms of PCOS and may pave the way for the development of control and therapeutic strategies for this condition in clinical practice. By bridging the gap between mouse models and clinical patients, this review contributes to a better understanding of the interplay between gut microbiota and inflammation in PCOS, thus paving new ways for future investigations and interventions.

Attention-deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental condition that persists into adulthood in the majority of individuals. While the gut-microbiome seems to be relevant for ADHD, the few publications on gut-microbial alterations in ADHD are inconsistent, in the investigated phenotypes, sequencing method/region, preprocessing, statistical approaches, and findings. To identify gut-microbiome alterations in adult ADHD, robust across studies and statistical approaches, we harmonized bioinformatic pipelines and analyses of raw 16S rRNA sequencing data from four adult ADHD case-control studies (NADHD=312, NNoADHD=305). We investigated diversity and differential abundance of selected genera (logistic regression and ANOVA-like Differential Expression tool), corrected for age and sex, and meta-analyzed the study results. Converging results were investigated for association with hyperactive/impulsive and inattentive symptoms across all participants. Beta diversity was associated with ADHD diagnosis but showed significant heterogeneity between cohorts, despite harmonized analyses. Several genera were robustly associated with adult ADHD; e.g., Ruminococcus_torques_group (LogOdds=0.17, pfdr=4.42 × 10-2), which was more abundant in adults with ADHD, and Eubacterium_xylanophilum_group (LogOdds= -0.12, pfdr=6.9 × 10-3), which was less abundant in ADHD. Ruminococcus_torques_group was further associated with hyperactivity/impulsivity symptoms and Eisenbergiella with inattention and hyperactivity/impulsivity (pfdr<0.05). The literature points towards a role of these genera in inflammatory processes. Irreproducible results in the field of gut-microbiota research, due to between study heterogeneity and small sample sizes, stress the need for meta-analytic approaches and large sample sizes. While we robustly identified genera associated with adult ADHD, that might overall be considered beneficial or risk-conferring, functional studies are needed to shed light on these properties.

Infertility is a disease of impaired fertility. With socioeconomic development, changes in human lifestyles, and increased environmental pollution, the problem of low human fertility has become increasingly prominent. The incidence of global infertility is increasing every year. Many factors lead to infertility, and common female factors include tubal factors, ovulation disorders, endometriosis, and immune factors. The gut microbiota is involved in many physiological processes, such as nutrient absorption, intestinal mucosal growth, glycolipid metabolism, and immune system regulation. An altered gut flora is associated with female infertility disorders such as polycystic ovary syndrome (PCOS), endometriosis (EMs), and premature ovarian failure (POF). Dysbiosis of the gut microbiota directly or indirectly contributes to the development of female infertility disorders, which also affect the homeostasis of the gut microbiota. Identifying the etiology and pathogenesis of infertility in patients is the focus of reproductive medicine physicians. We studied the developmental mechanism between the gut microbiota and PCOS, EMs, and POF from a new perspective, providing new ideas for diagnosing and treating female infertility diseases and specific reference values for eugenics.

Cardiovascular diseases (CVDs) are the leading cause of premature morbidity and mortality globally. The identification of novel risk factors contributing to CVD onset and progression has enabled an improved understanding of CVD pathophysiology. In addition to the conventional risk factors like high blood pressure, diabetes, obesity and smoking, the role of gut microbiome and intestinal microbe-derived metabolites in maintaining cardiovascular health has gained recent attention in the field of CVD pathophysiology. The human gastrointestinal tract caters to a highly diverse spectrum of microbes recognized as the gut microbiota, which are central to several physiologically significant cascades such as metabolism, nutrient absorption, and energy balance. The manipulation of the gut microbial subtleties potentially contributes to CVD, inflammation, neurodegeneration, obesity, and diabetic onset. The existing paradigm of studies suggests that the disruption of the gut microbial dynamics contributes towards CVD incidence. However, the exact mechanistic understanding of such a correlation from a signaling perspective remains elusive. This review has focused upon an in-depth characterization of gut microbial metabolites and their role in varied pathophysiological conditions, and highlights the potential molecular and signaling mechanisms governing the gut microbial metabolites in CVDs. In addition, it summarizes the existing courses of therapy in modulating the gut microbiome and its metabolites, limitations and scientific gaps in our current understanding, as well as future directions of studies involving the modulation of the gut microbiome and its metabolites, which can be undertaken to develop CVD-associated treatment options. Clarity in the understanding of the molecular interaction(s) and associations governing the gut microbiome and CVD shall potentially enable the development of novel druggable targets to ameliorate CVD in the years to come.

The human microbiome is a diverse ecosystem of microorganisms that reside in the body and influence various aspects of health and well-being. Recent advances in sequencing technology have brought to light microbial communities in organs and tissues that were previously considered sterile. The gut microbiota plays an important role in host physiology, including metabolic functions and immune modulation. Disruptions in the balance of the microbiome, known as dysbiosis, have been linked to diseases such as cancer, inflammatory bowel disease and metabolic disorders. In addition, the administration of antibiotics can lead to dysbiosis by disrupting the structure and function of the gut microbial community. Targeting strategies are the key to rebalancing the microbiome and fighting disease, including cancer, through interventions such as probiotics, fecal microbiota transplantation (FMT), and bacteria-based therapies. Future research must focus on understanding the complex interactions between diet, the microbiome and cancer in order to optimize personalized interventions. Multidisciplinary collaborations are essential if we are going to translate microbiome research into clinical practice. This will revolutionize approaches to cancer prevention and treatment.

Observational studies suggest associations between gut microbiota and polymyositis (PM) and dermatomyositis (DM), but causal relationships are unclear. We investigate the causal effects of gut microbiota on PM and DM, providing insights hoping to provide insights for future treatment and prevention.

Summary statistics of gut microbiota were obtained from a multi-ethnic Genome Wide Association Studies (GWAS) meta-analysis, including 119 taxa from 18,340 Europeans. PM/DM statistics were extracted from GWAS analyses. Mendelian randomization (MR) with IVW, MR-Egger, and weighted median methods was performed. Sensitivity analyses addressed heterogeneity and pleiotropy. Of the 119 bacterial genera studied, six showed causal links.

Alloprevotella (OR: 3.075, 95% CI: 1.127-8.386, p = 0.028), Ruminococcaceae UCG003 (OR: 4.219, 95% CI: 1.227-14.511, p = 0.022), Dialister (OR: 0.273, 95% CI: 0.077-0.974, p = 0.045) were associated with PM. Anaerotruncus (OR: 0.314, 95% CI: 0.112-0.882, p = 0.028), Ruminococcaceae UCG002 (OR: 2.439, 95% CI: 1.173-5.071, p = 0.017), Sutterella (OR: 3.392, 95% CI: 1.302-8.839, p = 0.012) were related to DM. Sensitivity analyses validated these associations.

We establish causal relationships between Ruminococcaceae, Sutterella, Anaerotruncus with DM, Alloprevotella, Ruminococcaceae UCG003, and Dialister with PM. Common microbiota, like Ruminococcaceae, have significant clinical implications. These findings open up greater possibilities for the gut microbiota to contribute to the development of PM/DM and for future monitoring of the gut microbiota in patients with PM/DM.

(1) Background: Dietary fiber can significantly alter gut microbiota composition. The role of the gut microbiome in the Gut-Brain Axis and modulation of neuropsychiatric disease is increasingly recognized. The role of antenatal diet, particularly fiber intake, in mitigating maternal mental health disorders remains unexplored. The objective of this review is to investigate the association between maternal fiber intake and perinatal depression and anxiety (PDA). (2) Methods: A literature review of PubMed and Google Scholar was conducted using appropriate keyword/MeSH terms for pregnancy, diet, fiber, and mental health. Observational and clinical trials published between 2015 and 2021 were included and data pertaining to dietary patterns (DP), food intake, mental health, and demographic data were extracted. The top three fiber-containing food groups (FG) per study were identified using a sum rank scoring system of fiber per 100 g and fiber per serving size. The consumption of these top three fiber FGs was then ranked for each dietary pattern/group. Mental health outcomes for each study were simplified into three categories of improved, no change, and worsened. The relationship between top three fiber FGs consumed within each DP and mental health outcomes was analyzed using Spearman's correlation. (3) Results: Thirteen of fifty-two studies met the inclusion criteria. Ten (76.9%) studies assessed DPs (seven examined depression only, two examined depression and anxiety, and one examined anxiety only). Seven (53.9%) studies reported at least one significant positive relationship between mental health outcomes and DPs while three reported at least one negative outcome. Three (23.1%) studies compared intake of different food groups between depressed and non-depressed groups. In studies of DPs, the average consumption ranking of the top three fiber FGs bore a significant inverse association with mental health outcomes [r = -0.419 (95%CI: -0.672--0.078)] p = 0.015. In studies comparing the intake of different FGs between depressed and non-depressed groups, the consumption of top-ranking fiber foods was higher in the non-depressed groups, but significantly higher in four of the ten high fiber FGs. (4) Conclusions: This study reframes findings from previously published studies of maternal diet and mental health outcomes to focus on fiber intake specifically, using a fiber ranking system. A significant correlation between lower intake of fiber and poorer mental health outcomes warrants further investigation in future studies.

Hypochlorous acid (HOCl) is an endogenous oxidant and chlorinating agent in mammals that is effective against a broad range of microorganisms. However, the effects of exogenous HOCl on biological processes have not been reported. In this study, the effects of highly purified slightly acidic hypochlorous acid water (HP-HAW) were investigated. After the safety of oral administration of HP-HAW was confirmed, the effects of HP-HAW on glucose homeostasis were assessed in mice. HP-HAW treatment significantly improved blood glucose levels in hyperglycemic condition. Based on the 16S rRNA sequencing, HP-HAW treatment significantly increased the diversity and changed the composition of gut microbiota by decreasing the abundance of genus Romboutsia in mice fed normal chow. In obese mice, HP-HAW administration tended to improve glucose tolerance. HP-HAW also attenuated memory impairments and changes N-methyl-d-aspartate (NMDA) receptor mRNA expression in obese mice. HP-HAW treatment suppressed Il-6 mRNA expression in the hippocampus in type 2 diabetic mice. Overall, these results support HP-HAW as a potential therapeutic agent to improve or prevent glucose tolerance and memory decline via gut microbiota alteration.

This study examined the effects of tocotrienols (TT) in conjunction with statin on glucose homeostasis, bone microstructure, gut microbiome, and systemic and liver inflammatory markers in obese C57BL/6J mice.

Forty male C57BL/6J mice were fed a high-fat diet (HFD) and assigned into four groups in a 2 (no statin vs. 120 mg statin/kg diet)×2 (no TT vs. 400 mg TT/kg diet) factorial design for 14 weeks.

Statin and TT improved glucose tolerance only when each was given alone, and only statin supplementation decreased insulin resistance. Consistently, only statin supplementation decreased serum insulin levels and HOMA-IR. Pancreatic insulin was also increased with statin treatment. Statin and TT, alone or in combination, reduced the levels of serum IL-6, but only TT attenuated the increased serum leptin levels induced by a HFD. Statin supplementation increased bone area/total area and connectivity density at LV-4, while TT supplementation increased bone area/total area and trabecular number, but decreased trabecular separation at the distal femur. Statin supplementation, but not TT, reduced hepatic inflammatory cytokine gene expression. Neither TT supplementation nor statin supplementation statistically altered microbiome species evenness or richness. However, they altered the relative abundance of certain microbiome species. Most notably, both TT and statin supplementation increased the relative abundance of Lachnospiraceae UCG-006.

TT and statin collectively benefit bone microstructure, glucose homeostasis, and microbial ecology in obese mice. Such changes may be, in part, associated with suppression of inflammation in the host.

Periodontal disease (PerioD) is a chronic inflammatory disease of dysbiotic etiology. Animal models and few human data showed a relationship between oral bacteria and gut dysbiosis. However, the effect of periodontal inflammation and subgingival dysbiosis on the gut is unknown. We hypothesized that periodontal inflammation and its associated subgingival dysbiosis contribute to gut dysbiosis even in subjects free of known gut disorders. We evaluated and compared elderly subjects with Low and High periodontal inflammation (assessed by Periodontal Inflamed Surface Area (PISA)) for stool and subgingival derived bacteria (assayed by 16S rRNA sequencing). The associations between PISA/subgingival dysbiosis and gut dysbiosis and bacteria known to produce short-chain fatty acid (SCFA) were assessed. LEfSe analysis showed that, in Low PISA, species belonging to Lactobacillus, Roseburia, and Ruminococcus taxa and Lactobacillus zeae were enriched, while species belonging to Coprococcus, Clostridiales, and Atopobium were enriched in High PISA. Regression analyses showed that PISA associated with indicators of dysbiosis in the gut mainly reduced abundance of SCFA producing bacteria (Radj = -0.38, p = 0.03). Subgingival bacterial dysbiosis also associated with reduced levels of gut SCFA producing bacteria (Radj = -0.58, p = 0.002). These results suggest that periodontal inflammation and subgingival microbiota contribute to gut bacterial changes.

The respiratory tract microbiome is essential for human health and well-being and is determined by genetic, lifestyle, and environmental factors. Patients with Common Variable Immunodeficiency (CVID) suffer from respiratory and intestinal tract infections, leading to chronic diseases and increased mortality rates. While CVID patients' gut microbiota have been analyzed, data on the respiratory microbiome ecosystem are limited.

This study aims to analyze the bacterial composition of the oropharynx of adults with CVID and its link with clinical and immunological features and risk for respiratory acute infections.

Oropharyngeal samples from 72 CVID adults and 26 controls were collected in a 12-month prospective study. The samples were analyzed by metagenomic bacterial 16S ribosomal RNA sequencing and processed using the Quantitative Insights Into Microbial Ecology (QIME) pipeline. Differentially abundant species were identified and used to build a dysbiosis index. A machine learning model trained on microbial abundance data was used to test the power of microbiome alterations to distinguish between healthy individuals and CVID patients.

Compared to controls, the oropharyngeal microbiome of CVID patients showed lower alpha- and beta-diversity, with a relatively increased abundance of the order Lactobacillales, including the family Streptococcaceae. Intra-CVID analysis identified age >45 years, COPD, lack of IgA, and low residual IgM as associated with a reduced alpha diversity. Expansion of Haemophilus and Streptococcus genera was observed in patients with undetectable IgA and COPD, independent from recent antibiotic use. Patients receiving azithromycin as antibiotic prophylaxis had a higher dysbiosis score. Expansion of Haemophilus and Anoxybacillus was associated with acute respiratory infections within six months.

CVID patients showed a perturbed oropharynx microbiota enriched with potentially pathogenic bacteria and decreased protective species. Low residual levels of IgA/IgM, chronic lung damage, anti antibiotic prophylaxis contributed to respiratory dysbiosis.

Understanding the relationship between dietary fat and physiological responses is crucial in species adapted to arid environments where water scarcity is common. In this study, we present a comprehensive exploration of gene expression across five tissues (kidney, liver, lung, gastrointestinal tract, and hypothalamus) and 19 phenotypic measurements, investigating the effects of dietary fat in the desert-adapted cactus mouse ( Peromyscus eremicus ). We show impacts on immune function, circadian gene regulation, and mitochondrial function for mice fed a lower-fat diet compared to mice fed a higher-fat diet. In arid environments with severe water scarcity, even subtle changes in organismal health and water balance can affect physical performance, potentially impacting survival and reproductive success. The study sheds light on the complex interplay between diet, physiological processes, and environmental adaptation, providing valuable insights into the multifaceted impacts of dietary choices on organismal well-being and adaptation strategies in arid habitats.

Diabetes mellitus (DM) is a chronic metabolic disorder characterized by an elevated level of blood glucose due to the absence of insulin secretion, ineffectiveness, or lack of uptake of secreted insulin in the body. The improperly diagnosed and poorly managed DM can cause severe damage to organs in the body like the nerves, eyes, heart, and kidneys. This study was aimed at investigating the effect of Clostridium butyricum (probiotic) with magnesium supplementation to evaluate the effect on gut microbial dysbiosis and blood glucose levels. In the laboratory, 6-8 weeks old 24 male albino rats weighing 200-250 g were given free access to water and food. Diabetes was induced using streptozotocin (60 mg/kg) in overnight fasted rats. Diabetic rats were randomly divided into four groups (n = 6, 6 replicates in each group). Metformin (100 mg/kg/day) with a standard basal diet was provided to control group (G0), Clostridium butyricum (1.5 × 105 CFU/day) with standard basal diet was provided to treatment group (G1), magnesium (500 mg/kg/day) was provided to group (G2). Clostridium butyricum (1.5 × 105 CFU/day) and magnesium (300 mg/kg/day) in combination with a standard basal diet was provided to group (G3). Blood Glucose, Magnesium blood test and microbial assay were done. Random blood glucose levels were monitored twice a week for 21 days and were represented as mean of each week. The results conclude that Clostridium butyricum (1.5 × 105 CFU) is very effective in balancing random blood glucose levels from 206.6 ± 67.7 to 85.1 ± 3.8 (p = 0.006) compared to other groups (p > 0.005). The results of stool analysis showed that Clostridium butyricum as probiotic restores microbial dysbiosis as evident by the 105 CFU Clostridium butyricum load in G1, which was higher than G0, G2 and G3 which were 103 and 104 CFU respectively. The findings of this study conclude that Clostridium butyricum supplementation improved blood glucose levels and intestinal bacterial load in type II diabetes mellitus.

Nutrition is one of the most influential environmental factors in both taxonomical shifts in gut microbiota as well as in the development of type 2 diabetes mellitus (T2DM). Emerging evidence has shown that the effects of nutrition on both these parameters is not mutually exclusive and that changes in gut microbiota and related metabolites such as short-chain fatty acids (SCFAs) and branched-chain amino acids (BCAAs) may influence systemic inflammation and signaling pathways that contribute to pathophysiological processes associated with T2DM. With this background, our review highlights the effects of macronutrients, carbohydrates, proteins, and lipids, as well as micronutrients, vitamins, and minerals, on T2DM, specifically through their alterations in gut microbiota and the metabolites they produce. Additionally, we describe the influences of common food groups, which incorporate varying combinations of these macronutrients and micronutrients, on both microbiota and metabolic parameters in the context of diabetes mellitus. Overall, nutrition is one of the first line modifiable therapies in the management of T2DM and a better understanding of the mechanisms by which gut microbiota influence its pathophysiology provides opportunities for optimizing dietary interventions.

Secondary metabolites and phytochemicals in plant-based diets are known to possess properties that inhibit the development of several diseases including a variety of cancers of the aerodigestive tract. Berries are currently of high interest to researchers due to their high dietary source of phytochemicals. Black raspberries (BRB), Rubus occidentalis, are of special interest due to their rich and diverse composition of phytochemicals. In this review, we present the most up-to-date preclinical and clinical data involving berries and their phytochemicals in the chemoprevention of a variety of cancers and diseases. BRBs possess a variety of health benefits including anti-proliferative properties, anti-inflammatory activity, activation of pro-cell-death pathways, modulation of the immune response, microbiome modulation, reduction in oxidative stress, and many more. However, little has been done in both preclinical and clinical settings on the effects of BRB administration in combination with other cancer therapies currently available for patients. With the high potential for BRBs as chemopreventive agents, there is a need to investigate their potential in combination with other treatments to improve therapeutic efficacy.

Attention-deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental condition that persists into adulthood in the majority of individuals. While the gut-microbiome seems to be relevant for ADHD, the few publications on gut-microbial alterations in ADHD are inconsistent, in the investigated phenotypes, sequencing method/region, preprocessing, statistical approaches, and findings. To identify gut-microbiome alterations in adult ADHD, robust across studies and statistical approaches, we harmonized bioinformatic pipelines and analyses of raw 16S rRNA sequencing data from four adult ADHD case-control studies (N ADHD =312, N NoADHD =305). We investigated diversity and differential abundance of selected genera (logistic regression and ANOVA-like Differential Expression tool), corrected for age and sex, and meta-analyzed the study results. Converging results were investigated for association with hyperactive/impulsive and inattentive symptoms across all participants. Beta diversity was associated with ADHD diagnosis but showed significant heterogeneity between cohorts, despite harmonized analyses. Several genera were robustly associated with adult ADHD; e.g., Ruminococcus_torques_group (LogOdds=0.17, p fdr =4.42×10 -2 ), which was more abundant in adults with ADHD, and Eubacterium_xylanophilum_group (LogOdds= -0.12, p fdr =6.9 x 10 -3 ), which was less abundant in ADHD. Ruminococcus_torques_group was further associated with hyperactivity/impulsivity symptoms and Eisenbergiella with inattention and hyperactivity/impulsivity (p fdr <0.05). The literature points towards a role of these genera in inflammatory processes. Irreproducible results in the field of gut-microbiota research, due to between study heterogeneity and small sample sizes, stress the need for meta-analytic approaches and large sample sizes. While we robustly identified genera associated with adult ADHD, that might overall be considered beneficial or risk-conferring, functional studies are needed to shed light on these properties.

Smart capsules are developing at a tremendous pace with a promise to become effective clinical tools for the diagnosis and monitoring of gut health. This field emerged in the early 2000s with a successful translation of an endoscopic capsule from laboratory prototype to a commercially viable clinical device. Recently, this field has accelerated and expanded into various domains beyond imaging, including the measurement of gut physiological parameters such as temperature, pH, pressure and gas sensing, and the development of sampling devices for better insight into gut health. In this review, the status of smart capsules for sensing gut parameters is presented to provide a broad picture of these state-of-the-art devices while focusing on the technical and clinical challenges the devices need to overcome to realise their value in clinical settings. Smart capsules are developed to perform sensing operations throughout the length of the gut to better understand the body's response under various conditions. Furthermore, the prospects of such sensing devices are discussed that might help readers, especially health practitioners, to adapt to this inevitable transformation in healthcare. As a compliment to gut sensing smart capsules, significant amount of effort has been put into the development of robotic capsules to collect tissue biopsy and gut microbiota samples to perform in-depth analysis after capsule retrieval which will be a game changer for gut health diagnosis, and this advancement is also covered in this review. The expansion of smart capsules to robotic capsules for gut microbiota collection has opened new avenues for research with a great promise to revolutionise human health diagnosis, monitoring and intervention.

With the establishment of the cardiac-gut axis concept, increasing evidence has suggested the involvement and important regulatory role of the gut microbiota (GM) and short chain fatty acid (SCFA) in cardiovascular diseases. However, the relationship between GM and atrial fibrillation (AF) is still poorly understood.

The aim of this study was to investigate whether there were differences in GM and SCFA between AF patients and healthy controls.

In this study, we enrolled 30 hospitalized patients with AF and 30 matched patients with sinus rhythm (SR). GM species in fecal samples were evaluated through amplicon sequencing targeting the 16Sribosomal RNA gene. The feces SCFAs were describe step by step the quantitative analysis using gas chromatography-mass spectrometry (GC-MS). GM species richness, diversity, differential abundance of individual taxa between AF and SR were analyzed.

AF patients showed decreased species richness and α-diversity compared to SR patients, but there was no statistical difference. The phylogenetic diversity was significant decreased in AF group. The β-diversity indexes revealed significant differences in GM community structure between the AF group and the SR group. After investigated the individual taxa, AF group showed altered relative abundance in several taxa compared to the SR group. linear discriminant analysis (LDA) effect size (LEfSe) analysis revealed, a significant decrease in Bifidobacterium and a greater abundance of Lactobacillus, Fusobacterium, Haemophilus in AF group compared with the SR group. The abundance of haemophilus was negative correlated with isovaleric acid and isobutyric acid.

In AF patients, the GM phylogenetic diversity and β-diversity decreased, the relative abundance altered in several taxa and the bacterial community structure changed as well as the SCFA level. GM and SCFA dysbiosis might play a crucial part in the occurrence and development of AF.

As a rapidly growing field, microbiota research offers novel approaches to promoting ocular health and treating major retinal diseases, such as glaucoma. Gut microbiota changes throughout life; however, certain patterns of population changes have been increasingly associated with specific diseases. It has been well established that a disrupted microbiome contributes to central nervous system diseases, including Alzheimer disease, Parkinson disease, multiple sclerosis, and glioma, suggesting a prominent role of microbiome in neurodegenerative diseases. This review summarizes the progress in identifying significant changes in the microbial composition of patients with glaucoma by compiling studies on the association between microbiota and disease progression. Of interest is the relationship between increased Firmicutes/Bacteroidetes ratio in patients with primary open-angle glaucoma, increased taurocholic acid, decreased glutathione, and a reduction in retinal ganglion cell survival. Connecting these microbes to specific metabolites sheds light on the pathogenic mechanism and novel treatment strategies. In summary, the current review synthesizes the findings of several studies investigating the effects of shifting bacterial population in retinal diseases, particularly glaucoma, with the aim to identify the current direction of treatment and help direct future endeavors.

In recent years, the role of new factors in the pathophysiology of neurodegenerative diseases has been investigated. Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common neurodegenerative diseases worldwide. Although pathological changes such as the accumulation of aggregated proteins in the brain and inflammatory responses are known as the main factors involved in the development of these diseases, new studies show the role of gut microbiota and circadian rhythm in the occurrence of these changes. However, the association between circadian rhythm and gut microbiota in AD and PD has not yet been investigated. Recent results propose that alterations in circadian rhythm regulators, mainly Bmal1, may regulate the abundance of gut microbiota. This correlation has been linked to the regulation of the expression of immune-related genes and Bmal-1 mediated oscillation of IgA and hydrogen peroxide production. These data seem to provide new insight into the molecular mechanism of melatonin inhibiting the progression of AD and PD. Therefore, this manuscript aims to review the role of the gut microbiota and circadian rhythm in health and AD and PD and also presents a hypothesis on the effect of melatonin on their communication.

To explore the effect of ultra-strong static magnetic field on gut microbiota, 16 T static magnetic field was used to study the changes in the structure and composition of human and mouse gut microbiota in this environment. In the mouse gut microbiota, at the genus level, the magnetic field significantly decreased the relative abundances of Escherichia-Shigella, Lactobacillus, Enterococcus, Burkholderia-Caballeronia-Paraburkholderia, Parasutterella, and Ralstonia and significantly increased those of Parabacteroides, Alloprevotella, Alistipes, Odoribacter, Bacteroides, Mucispirillum, Sutterella, and Prevotellaceae_UCG-001. Similarly, at the genus level, the relative abundances of Bacteroides, Parabacteroides, Romboutsia, and Streptococcus significantly decreased in the human gut microbiota. Contrary to the changing trend of the abundance in the mouse gut, the abundances of Bacteroides and Parabacteroides in the human gut were significantly reduced under magnetic field. The BugBase phenotypic prediction analysis showed that the relative abundances of five phenotypes, including anaerobism, mobile elements, potential pathogenicity, stress-tolerant, and biofilm formation, changed significantly in the mouse gut microbiota, while the relative abundances of two phenotypes, including Gram-positive and Gram-negative phenotypes, changed significantly in the human gut microbiota. The 16 T magnetic field could differently affect the composition, structure, and phenotypes of gut microbiota in human and mice, suggesting the importance of model selection in studying the biological effects of magnetic field.

Tuberculosis (TB), an airborne pulmonary disease caused by Mycobacterium tuberculosis (M. tb), poses an unprecedented health and economic burden to most of the developing countries. Treatment of TB requires prolonged use of a cocktail of antibiotics, which often manifest several side effects, including stomach upset, nausea, and loss of appetite spurring on treatment non-compliance and the emergence of antibiotic resistant M. tb. The anti-TB treatment regimen causes imbalances in the composition of autochthonous microbiota associated with the human body, which also contributes to major side effects. The microbiota residing in the gastrointestinal tract play an important role in various physiological processes, including resistance against colonization by pathogens, boosting host immunity, and providing key metabolic functions. In TB patients, due to prolonged exposure to anti-tuberculosis drugs, the gut microbiota significantly loses its diversity and several keystone bacterial taxa. This loss may result in a significant reduction in the functional potency of the microbiota, which is a probable reason for poor treatment outcomes. In this review, we discuss the structural and functional changes of the gut microbiota during TB and its treatment. A major focus of the review is oriented to the gut microbial association with micronutrient profiles and immune cell dynamics during TB infection. Furthermore, we summarize the acquisition of anti-microbial resistance in M. tb along with the microbiome-based therapeutics to cure the infections. Understanding the relationship between these components and host susceptibility to TB disease is important to finding potential targets that may be used in TB prevention, progression, and cure.

Adult humans harbor at least as many microbial cells as eukaryotic ones. The largest compartment of this diverse microbial population, the gut microbiota, encompasses the collection of bacteria, archaea, viruses, and eukaryotic organisms that populate the gastrointestinal tract, and represents a complex and dynamic ecosystem that has been increasingly implicated in health and disease. The gut microbiota carries ∼100-to-150-times more genes than the human genome and is intimately involved in development, homeostasis, and disease. Of the several microbial metabolites that have been studied, short-chain fatty acids emerge as a group of molecules that shape gene expression in several types of eukaryotic cells by multiple mechanisms, which include DNA methylation changes, histone post-translational modifications, and microRNA-mediated gene silencing. Butyric acid, one of the most extensively studied short-chain fatty acids, reaches higher concentrations in the colonic lumen, where it provides a source of energy for healthy colonocytes, and its concentrations decrease towards the bottom of the colonic crypts, where stem cells reside. The lower butyric acid concentration in the colonic crypts allows undifferentiated cells, such as stem cells, to progress through the cell cycle, pointing towards the importance of the crypts in providing them with a protective niche. In cancerous colonocytes, which metabolize relatively little butyric acid and mostly rely on glycolysis, butyric acid preferentially acts as a histone deacetylase inhibitor, leading to decreased cell proliferation and increased apoptosis. A better understanding of the interface between the gut microbiota metabolites and epigenetic changes in eukaryotic cells promises to unravel in more detail processes that occur physiologically and as part of disease, help develop novel biomarkers, and identify new therapeutic modalities.

With very little research exploring intestinal effects of red beetroot consumption, the present pilot study investigated gut microbial changes following red beetroot consumption, via a 14-day intervention trial in healthy adults. Compared to baseline, the study demonstrates transient changes in abundance of some taxa e.g., Romboutsia and Christensenella, after different days of intervention (p < 0.05). Enrichment of Akkermansia muciniphila and decrease of Bacteroides fragilis (p < 0.05) were observed after 3 days of juice consumption, followed by restoration in abundance after 14 days. With native betacyanins and catabolites detected in stool after juice consumption, betacyanins were found to correlate positively with Bifidobacterium and Coprococcus, and inversely with Ruminococcus (p < 0.1), potentiating a significant rise in (iso)butyric acid content (172.7 ± 30.9 µmol/g stool). Study findings indicate the potential of red beetroot to influence gut microbial populations and catabolites associated with these changes, emphasizing the potential benefit of red beetroot on intestinal as well as systemic health.

The human gut microbiota, a complex community of microorganisms living in the digestive tract, consists of more than 1500 species distributed in more than 50 different phyla, with 99% of bacteria coming from about 30-40 species. The colon alone, which contains the largest population of the diverse human microbiota, can harbor up to 100 trillion bacteria. The gut microbiota is essential in maintaining normal gut physiology and health. Therefore, its disruption in humans is often associated with various pathological conditions. Different factors can influence the composition and function of the gut microbiota, including host genetics, age, antibiotic treatments, environment, and diet. The diet has a marked effect, impacting the gut microbiota composition, beneficially or detrimentally, by altering some bacterial species and adjusting the metabolites produced in the gut environment. With the widespread use of non-nutritive sweeteners (NNS) in the diet, recent investigations have focused on their effect on the gut microbiota as a mediator of the potential impact generated by gastrointestinal-related disturbances, such as insulin resistance, obesity, and inflammation. We summarized the results from pre-clinical and clinical studies published over the last ten years that examined the single effects of the most consumed NNS: aspartame, acesulfame-K, sucralose, and saccharin. Pre-clinical studies have given conflicting results for various reasons, including the administration method and the differences in metabolism of the same NNS among the different animal species. A dysbiotic effect of NNS was observed in some human trials, but many other randomized controlled trials reported a lack of significant impacts on gut microbiota composition. These studies differed in the number of subjects involved, their dietary habits, and their lifestyle; all factors related to the baseline composition of gut microbiota and their response to NNS. The scientific community still has no unanimous consensus on the appropriate outcomes and biomarkers that can accurately define the effects of NNS on the gut microbiota.

A growing body of evidence from multiple areas proposes that periodontal disease, accompanied by oral inflammation and pathological changes in the microbiome, induces gut dysbiosis and is involved in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). A subgroup of NAFLD patients have a severely progressive form, namely nonalcoholic steatohepatitis (NASH), which is characterized by histological findings that include inflammatory cell infiltration and fibrosis. NASH has a high risk of further progression to cirrhosis and hepatocellular carcinoma. The oral microbiota may serve as an endogenous reservoir for gut microbiota, and transport of oral bacteria through the gastro-intestinal tract can set up a gut microbiome dysbiosis. Gut dysbiosis increases the production of potential hepatotoxins, including lipopolysaccharide, ethanol, and other volatile organic compounds such as acetone, phenol and cyclopentane. Moreover, gut dysbiosis increases intestinal permeability by disrupting tight junctions in the intestinal wall, leading to enhanced translocation of these hepatotoxins and enteric bacteria into the liver through the portal circulation. In particular, many animal studies support that oral administration of Porphyromonas gingivalis, a typical periodontopathic bacterium, induces disturbances in glycolipid metabolism and inflammation in the liver with gut dysbiosis. NAFLD, also known as the hepatic phenotype of metabolic syndrome, is strongly associated with metabolic complications, such as obesity and diabetes. Periodontal disease also has a bidirectional relationship with metabolic syndrome, and both diseases may induce oral and gut microbiome dysbiosis with insulin resistance and systemic chronic inflammation cooperatively. In this review, we will describe the link between periodontal disease and NAFLD with a focus on basic, epidemiological, and clinical studies, and discuss potential mechanisms linking the two diseases and possible therapeutic approaches focused on the microbiome. In conclusion, it is presumed that the pathogenesis of NAFLD involves a complex crosstalk between periodontal disease, gut microbiota, and metabolic syndrome. Thus, the conventional periodontal treatment and novel microbiome-targeted therapies that include probiotics, prebiotics and bacteriocins would hold great promise for preventing the onset and progression of NAFLD and subsequent complications in patients with periodontal disease.

The prevalence of anxiety and depression soared following the COVID-19 pandemic. To effectively treat these conditions, a comprehensive understanding of all etiological factors is needed. This study investigated fecal microbial features associated with mental health outcomes (symptoms of anxiety, depression, or posttraumatic stress disorder (PTSD)) in a Spanish cohort in the aftermath of the COVID-19 pandemic. Microbial communities from stool samples were profiled in 198 individuals who completed validated, self-report questionnaires. 16S ribosomal RNA gene V3-4 amplicon sequencing was performed. Microbial diversity and community structure were analyzed, together with relative taxonomic abundance. In our cohort of N=198, 17.17% reported depressive symptoms, 37.37% state anxiety symptoms, 40.90% trait anxiety symptoms, and 8.08% PTSD symptoms, with high levels of comorbidity. Individuals with trait anxiety had lower Simpson's diversity. Fusicatenibacter saccharivorans was reduced in individuals with comorbid PTSD + depression + state and trait anxiety symptoms, whilst an expansion of Proteobacteria and depletion of Synergistetes phyla were noted in individuals with depressive symptoms. The relative abundance of Anaerostipes was positively correlated with childhood trauma, and higher levels of Turicibacter sanguinis and lower levels of Lentisphaerae were found in individuals who experienced life-threatening traumas. COVID-19 infection and vaccination influenced the overall microbial composition and were associated with distinct relative taxonomic abundance profiles. These findings will help lay the foundation for future studies to identify microbial role players in symptoms of anxiety, depression, and PTSD and provide future therapeutic targets to improve mental health outcomes.

Gut microbiota was only considered as a commensal organism that aids in digestion, but recent studies revealed that the microbiome play a critical role in both physiological and pathological immune system. The gut microbiome composition is altered by environmental factors such as diet and hygiene, and the alteration affects immune cells, especially T cells. Advanced genomic techniques in microbiome research defined that specific microbes regulate T cell responses and the pathogenesis of immune-mediated disorders. Here, we review features of specific microbes-T cell crosstalk and relationship between the microbes and immunopathogenesis of diseases including in cancers, autoimmune disorders and allergic inflammations. We also discuss the limitations of current experimental animal models, cutting-edge developments and current challenges to overcome in the field, and the possibility of considering gut microbiome in the development of new drug.

This work aimed to observe the effect of consuming Chinese herb tea on glucolipid metabolism and gut microbiota in patients with type 2 diabetes mellitus (T2DM).

Ninety patients with T2DM were recruited from a community and randomly divided into the control group (CG) and intervention group (IG). CG maintained conventional treatment and lifestyle, and IG accepted additional "maccog" traditional Chinese medicine (TCM) tea (mulberry leaf, radix astragali, corn stigma, cortex lycii, radix ophiopogonis, and gynostemma) for 12 weeks. Glucolipid metabolism, hepatorenal function, and gut microbiota were then measured.

After the intervention, the decreases in fasting plasma glucose (FPG) and total cholesterol (TC) were greater (P<0.05) in IG than in CG, and those in glycosylated serum protein (GSP) were almost significantly greater (P=0.066) in IG than in CG. The total protein (TP), albumin (ALB), and creatinine (CREA) levels in IG were significantly lower and their decreases were larger in IG than in CG (P<0.05) after the intervention. The Ace and Chao1 indices in IG were slightly higher after the intervention (P=0.056 and 0.052, respectively) than at baselines. The abundance of Actinobacteria, Lachnospiraceae, Bifidobacteriaceae, and Phascolarctobacterium increased significantly after the intervention in IG (P<0.05), and the abundance was higher in IG than in CG (P<0.05 or P<0.1). The abundance of Clostridiales and Lactobacillales was negatively correlated with FPG (P<0.05), Clostridiales and Lachnospiraceae was negatively correlated with GSP (P<0.05), and Bacteroides/Firmicutes was positively correlated with both (P<0.05). No adverse event was observed during the intervention.

Administration of "maccog" TCM tea for 12 weeks slightly improved glucolipid metabolism and significantly increased the abundance of beneficial gut microbiota in community patients with T2DM. The increase in beneficial bacteria abundance may be involved in the improvement of glucose metabolism indicators. In addition, this intervention is safe and feasible.

https://www.chictr.org.cn/showproj.aspx?proj=31281, identifier ChiCTR1800018566.