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Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Jul 15, 2024; 15(7): 1409-1416
Published online Jul 15, 2024. doi: 10.4239/wjd.v15.i7.1409
Diabetes and tuberculosis: An emerging dual threat to healthcare
Sahana Shetty, Department of Endocrinology, Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal 576104, Karnataka, India
Joseph M Pappachan, Department of Endocrinology and Metabolism, Lancashire Teaching Hospitals NHS Trust, Preston PR2 9HT, United Kingdom
Joseph M Pappachan, Faculty of Science, Manchester Metropolitan University, Manchester M15 6BH, United Kingdom
Joseph M Pappachan, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester M13 9PL, United Kingdom
Cornelius James Fernandez, Department of Endocrinology & Metabolism, Pilgrim Hospital, United Lincolnshire Hospitals NHS Trust, Boston PE21 9QS, United Kingdom
ORCID number: Sahana Shetty (0000-0003-0851-0411); Joseph M Pappachan (0000-0003-0886-5255); Cornelius James Fernandez (0000-0002-1171-5525).
Author contributions: Shetty S and Fernandez CJ wrote the initial draft of the manuscript with some help from Pappachan JM by performing literature search, interpretation of relevant scientific data, and compiling the best evidence; Fernandez CJ also contributed to the critical revision, important intellectual content and figure preparation for the paper; Pappachan JM contributed to the conceptual design of the paper and provided additional input to the drafting, literature review, revision and modifications of the paper; all the authors have read and approved the final version of the manuscript.
Conflict-of-interest statement: Professor Joseph M Pappachan and co-authors have no conflicts to declare.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Joseph M Pappachan, MD, FRCP, Academic Editor, Professor, Department of Endocrinology and Metabolism, Lancashire Teaching Hospitals NHS Trust, Sharoe Green Lane, Preston PR2 9HT, United Kingdom. drpappachan@yahoo.co.in
Received: March 4, 2024
Revised: April 21, 2024
Accepted: April 24, 2024
Published online: July 15, 2024
Processing time: 125 Days and 18.8 Hours


Tuberculosis (TB) remains a huge global healthcare challenge even in the 21st century though the prevalence has dropped in developed countries in recent decades. Diabetes mellitus (DM) is an important risk factor for the development and perpetuation of TB owing to the immune dysfunction in patients with DM. The coexistence of both diseases in the same individual also aggravates disease severity, complications, and chance of treatment failure because of gross immune alterations posed by DM as well as TB. Various complex cellular and humoral immunological factors are involved in the dangerous interaction between TB and DM, some of which remain unknown even today. It is highly important to identify the risk factors for TB in patients with DM, and vice versa, to ensure early diagnosis and management to prevent complications from this ominous coexistence. In their research study published in the recent issue of the World Journal of Diabetes, Shi et al elaborate on the factors associated with the development of TB in a large cohort of DM patients from China. More such research output from different regions of the world is expected to improve our knowledge to fight the health devastation posed by TB in patients with diabetes.

Key Words: Tuberculosis, Diabetes mellitus, Immune dysfunction, Treatment failure, Multi-drug resistant tuberculosis

Core Tip: Tuberculosis (TB) and diabetes mellitus (DM) are two common diseases especially highly prevalent in developing countries. Diabetes is an important risk factor for the development and perpetuation of TB owing to the immune dysfunction in patients with DM, whereas TB-related cellular and immunological alterations can worsen diabetes control. It is crucial to identify the risk factors for TB in patients with DM and vice versa to ensure prompt diagnosis and optimal management. Shi et al recently elaborated the factors associated with development of TB in DM cases in a recent issue of World Journal of Diabetes. Such research data is expected to improve our knowledge to fight against these dangerous diseases.


Tuberculosis (TB) remains as a significant healthcare challenge in several developing countries even after the global effort to curtail the devastation of the disease under the leadership of international agencies like the United Nations and World Health Organisation (WHO) in the past few years. While undernutrition remains a major risk factor for TB-related morbidity and mortality in resource-poor settings[1], other comorbidities such as advanced kidney disease, human immunodeficiency virus infection and diabetes mellitus (DM) significantly increase the risk of onset and progression of TB[2]. Therefore, healthcare providers should be mindful of these risk factors while diagnosing and managing any patient with TB.

According to the Global Health Observatory of WHO, the median diabetes prevalence in 30 countries with high TB burden in 2021 was 8%, which is expected to increase by 99% by the year 2045[3]. Further, it suggests that DM is associated with a two- to three-fold excess risk of TB, a two-fold excess risk of treatment-related TB mortality, a four-fold higher risk of TB relapse following treatment and a two-fold excess risk of multi-drug resistant TB (MDR-TB). The pooled prevalence of diabetes in TB patients was estimated to be 21% in a meta-analysis of 74 studies from Southeast Asia, higher than in many other regions of the world[4]. The estimated global prevalence of DM in individuals with TB was > 15%, while the total diabetes prevalence was only 9.3% in the year 2019[5,6]. Therefore, an estimated 1.5 million patients worldwide need coordinated care to manage both DM and TB optimally[3].

TB and DM are most common in low- and middle-income nations and these countries report higher rates of TB and DM combination. Six of the ten nations with the largest number of DM patients globally are categorised by the WHO as having a "high burden" of TB, which means they are responsible for 80% of all TB cases globally[3]. Worldwide research on the epidemiology of TB-related diabetes is expanding, and Some areas, such as South India (54%), the Pacific Islands (40%) and northern Mexico (36%), show notably high prevalence rates of diabetes in patients with TB[5]. Understanding the pathobiology, clinical characteristics, appropriate management strategies, and follow-up care is crucial to ensure optimal disease-related clinical outcomes in patients with both conditions.


The relationship between TB and DM is bidirectional with each adversely impacting the other in a vicious cycle and compounding the clinical presentation and/or complications associated with them.

Impact of diabetes on TB

DM is an important risk factor for latent and active TB. Immunological alterations in patients with DM increase the susceptibility to developing active TB. Alterations in both innate and adaptive immune responses mediate the risk of TB in patients with DM[7]. The innate immune response is mediated by macrophages, dendritic cells (DCs), innate lymphoid cells (ILCs), and neutrophils. In contrast, the adaptive immune response is mediated by cytotoxic T lymphocytes (CTLs), T-helper type 1 (Th1), T-helper type 17 (Th17) and regulatory T cells (Tregs)[7]. The immune dysfunction occurs at various levels including T cell abnormalities with altered secretion of cytokines and chemokines, aberrations in innate immunity with impaired functions of neutrophils, macrophages and antigen-presenting cells, and bacterial recognition, abnormalities in B cell function with defective antibody production and alteration in the complement system[8].

Martinez et al[9] reported decreased expression of CD14 and MARCO (macrophage receptor with a collagenous structure – acts as a scavenger) in the alveolar macrophages which are involved in the recognition of mycobacterial cell wall components in hyperglycaemic mice, masking Mycobacterium tuberculosis (Mtb) recognition. DM decreases macrophage function by reducing HLA-DR expression, increasing PD-L1 expression [decreasing Th1 immune response and interferon-gamma (IFN-γ) production], increasing chemokine receptor 2 expression (decreasing monocyte homing to the lungs), and inducing lysosomal dysfunction (decreasing Mtb clearance)[7]. DM is also associated with reduced myeloid and plasmacytoid DC (mDC and pDC) numbers, reduced migration of DCs to lymph nodes for maturation, impaired ability to prime T cells, and thereby impaired Mtb clearance[10].

The chronic low-grade inflammation of DM is associated with increased interleukin (IL)-8, tumor necrosis factor (TNF) and IL-6 production and thereby neutrophil recruitment (neutrophilia)[11]. Raised resistin levels of DM impair the chemotactic function and reactive oxygen species (ROS) generation by neutrophils[12]. DM is associated with decreased ILC3 and increased ILC1 (also known as natural killer cells)[7]. The decreased IL-22 production by the lowered ILC3 frequency decreased the survival of Mtb-infected mice with DM[13]. Similarly, the increased IL-6 production by the raised ILC1 frequency decreased the CD4+ T cell proliferation, Th1 and Th17 immune response and thereby the survival of Mtb-infected mice with diabetes[14]. Though the Th1 number remains unchanged in DM, the Th1/Th2 ratio is decreased due to a marked increase in Th2 and Th17 cells[15]. This is associated with a reduction in Tregs and CD4+ & CD8+ T-cells[16]. Diabetes is associated with a reduction in IL-12 (promoter of Th1 response and IFN-γ production) and an increase in IL-10 (inhibitor of Th1 response), thereby reducing the IFN-γ, IL-2, and IL-1Ra production[17]. The resultant reduced IL-2 reduces the CTL activation and increases the T cell apoptosis[18]. Finally, the reduced IL-1Ra production increases the formation of pathogenic Th1/Th17 hybrid cells that are associated with worse active TB[19].

DM-induced abnormalities in the innate immune system permit easy invasion of respiratory epithelium by the Mtb and prolonged persistence. Abnormalities in the adaptive immune response in the form of dysregulation of the T cell profile and impaired B cell function promote chronic inflammation and granuloma formation[20]. Defective immune response facilitates both the development of primary TB and the reactivation of latent TB. This impaired immune response not only increases the risk of acquiring infection but also increases the severity of infection. The resulting higher bacterial load, poor inflammatory response, reduced bactericidal activity and dissemination may predispose to severe presentations, including the development of military TB[21]. Figure 1 depicts immune system abnormalities predisposing to TB infection and severe presentations of the disease in patients with DM.

Figure 1
Figure 1 Various immune system abnormalities predispose to tuberculosis infection and its severe course in patients with diabetes mellitus. ATB: Active tuberculosis; LTB: Latent tuberculosis; MDR-TB: Multi-drug resistant tuberculosis.
Impact of TB on glycemia

TB can cause or worsen existing hyperglycaemia. In a meta-analysis by Menon et al[22], newly developed hyperglycaemia was seen in 27.3% of TB patients at baseline. The hyperglycaemia persisted in 50% of subjects at 3-6 months of follow-up. Krishnappa et al[23] demonstrated the adverse impact of TB on glycemia - with 7% of TB patients developing a new diagnosis of DM and 4.5% developing impaired glucose tolerance (IGT). They also reported improvement in blood sugar levels at the end of successful treatment of TB, with 65% of IGT patients reverting to euglycemia following successful treatment of TB.

This hyperglycaemic effect is proposed as secondary to stress, prolonged inflammation, alterations in glucose and lipid metabolism, and the development of insulin resistance among patients with TB. The antitubercular drugs could also influence the pharmacokinetics and pharmacodynamics of the glucose-lowering therapies and worsen the complications of diabetes. Patients with TB and DM carry a higher risk of developing cardiovascular complications such as myocardial infarction and stroke as well as DVT during the early months of TB treatment[24].

Toll-like receptors (TLRs) enable macrophages to recognize various Mtb proteins[25]. Interaction of proline-proline-glutamic acid (PPE17) or protein Rv1168c of Mtb with TLR2[26] and Mtbhsp60 (heat shock protein 60 of Mtb) with TLR4[27], respectively results in nuclear factor kappa B (NF-kB) signalling, production of ROS and reactive nitrogen intermediates, and expression of pro-inflammatory cytokines including TNF-α and IL-6. Another Mtb protein known as Rv0183, a monoglyceride lipase (mtbMGL) from Mtb, induces myeloid differentiation factor 88 (MyD88)-NF-kB signalling and expression of pro-inflammatory IL-6 and TNF-α[28]. Yet another Mtb protein known as MTP53 (Rv2878c) directly interacts with, and activates transforming growth factor-β-activated kinase 1 or TAK1 independent of TLR2 or MyD88 to enhance pro-inflammatory cytokine expression[29]. Mtb-infected macrophages also secrete matrix metalloproteinases (MMPs), especially MMP-2 and MMP-9, which degrade the extracellular matrix components in the adipose tissue allowing adipocytes to hypertrophy[30].

The adipocyte hypertrophy decreases adiponectin but increases the leptin and resistin expression[21]. Resistin increases lipolysis by increasing the expression of hormone-sensitive lipase[31]. Acting via the mTORC2/Akt pathway in adipocytes, Mtb increases TNF-α and MCP-1[32], with the latter promoting inflammation by attracting monocytes and T lymphocytes[33]. The TNF-α activates protein kinase A, which in turn phosphorylates hormone-sensitive lipase, thereby causing lipolysis in the adipocytes[34]. Ectopic deposition of resultant free fatty acids results in the development of hepatic and skeletal muscle insulin resistance[34].

Mtb protein-TLR interaction on macrophages results in the stabilisation of hypoxia-mediated factor-1α (HIF-1α) in addition to NF-kB signalling and expression of pro-inflammatory cytokines[35]. HIF-1α induces the formation of lipid droplets (a risk factor for DM) and upregulates the glycolytic genes and genes for pro-inflammatory mediators like IL-1β[35]. Lipid droplets are also formed by the TNF-α produced during Mtb infection interacting with TNF receptor-associated factors[36] and various lipases (Rv3091, Rv0183, Rv1592c, Rv2037c, and Rv1683) produced by Mtb present inside the phagosomes[37]. These lipases metabolise host lipids to form fatty acids which are used as the source of energy, as building blocks for cell envelope and as regulators of host immune response. Fatty acids are also produced with the help of the Mtb protein known as ESAT-6 which increases the GLUT-1 (glucose transporter) mediated glucose uptake, upregulates the glycolytic genes, and downregulates the Kreb cycle genes in macrophages[38]. The resultant decreased mitochondrial respiration causes inflammation and thereby worsens insulin resistance[21]. Pyruvate from upregulated glycolysis is converted to lactate and secreted out of the cell. Excess pyruvate is transported into the mitochondria and enters the Kreb cycle resulting in the accumulation of citrate which, on return to the cytoplasm, is converted to acetyl-CoA to be fed into fatty acid biosynthesis[21]. Figure 2 shows the pathobiological aspects of macrophage and adipocyte interactions and the related cellular events perpetuating TB and DM.

Figure 2
Figure 2 Interactions between macrophages and adipocytes with the release of various cytokines and chemokines perpetuate tuberculosis and diabetes mellitus in disease-prone individuals. Mtb: Mycobacterium tuberculosis; TNF-α: Tumor necrosis factor; IL: Interleukin.

Mtb infection in patients with diabetes usually runs a severe clinical course with rapid progression and more severe pulmonary and extrapulmonary manifestations as compared to those without diabetes. Pulmonary TB can often be bilateral and extensive with cavitation and infiltration in those with DM[39]. They also have a higher mycobacterial load. Resistance to anti-tubercular drugs with genotypical drug resistance and late culture conversion are additional concerns in these patients[40]. They may have higher rates of treatment failure, relapse, and mortality compared to TB patients without diabetes. Studies have also reported a 2-fold higher mortality in TB patients with diabetes[41]. Patients with type 2 DM (T2DM) were found to have a 2-fold excess risk of developing MDR-TB[42,43]. Diabetes can also complicate the diagnosis of TB as it can mask some of the usual symptoms of TB or lead to atypical presentations, delaying diagnosis and treatment initiation. The level of HbA1c control has an influence on efficacy of anti-tuberculous therapy as measure by sputum conversion rate and TB focus absorption[44]. Finally, a rising HbA1c trend during and after anti-tuberculous therapy may be a predictor of adverse treatment response in those presenting with HbA1c ≥ 48 mmol/mol at the time of diagnosis of TB[45]. Thus, DM has an impact on the clinical presentation, severity, response to therapy and prognosis of TB.


A high index of clinical suspicion and prompt screening for TB in those with suggestive symptomatology is essential in patients with DM. The co-existence of TB and DM may interfere with the therapeutic intervention of both TB and DM and influence the response to therapies. Although the treatment approach to both Diabetes and TB would not differ significantly, it is important to be aware of drug interactions and to make appropriate modifications to the treatment regimens. It is important to achieve strict glycaemic control for the success of TB treatment. Frequent glucose monitoring and titration of drug doses would be vital to achieve strict control[46]. Steroids given for meningeal and pericardial TB increases the risk of causing hyperglycaemia and this needs to be monitored appropriately[47].

Given the interconnection between TB and diabetes, there is increasing recognition of the need for integrated care for individuals with both TB and diabetes. Measures could be taken for coordinated efforts between TB and diabetes programs to ensure optimal management of both diseases.


A coordinated approach for long-term care for DM coupled with immediate short-term care for TB management is vital in a successful therapeutic algorithm for patients with both diseases. Ensuring optimal glycaemic control assists in a better response to TB therapies. Compliance with both therapies must be assessed regularly with periodic follow-ups and appropriate testing.

TB and diabetes form a dangerous combination, each exacerbating the other's impact and complicating management. Hence, addressing both diseases together is crucial for better health outcomes. With an increasing diabetes prevalence in pandemic proportions across the globe, there is an urgent need for healthcare providers and professional bodies to be highly vigilant about the dangerous duo of DM and TB. Better preparedness at various levels of health care, a multidisciplinary approach, and coordinated efforts of Diabetes and TB management programs would help to address this dual threat.


Ongoing research is expected to shed more light on our knowledge base on the pathobiology, risk factors, prognostication, and management of patients with DM and TB. In their recent study published in the World Journal of Diabetes, Shi et al[48], report factors associated with risk for TB in patients with T2DM from a large cohort of patients from China. This study observed that T2DM subjects with poor glycaemic control, hypoproteinaemia, lymphopenia, history of TB contact, recurrent infections, smoking, and alcohol consumption were associated with an increased risk of developing pulmonary TB. In contrast, being in a married relationship, the presence of hypertension, oral hypoglycaemic agent plus insulin-treated T2DM, overweight, obesity and regular exercise were associated with a reduced risk of developing pulmonary TB in their univariate analysis. While lymphopenia [odds ratio (OR): 17.75], smoking (OR: 12.25), history of TB contact (OR: 6.56) and poor glycaemic control (OR: 3.37) were associated with an excess risk of developing pulmonary TB in patients with T2DM, being overweight (OR: 0.23) and obese (OR: 0.11) posed a lower risk in their multivariate analysis.

The study by Shi et al[48], used a 1:2 ratio case-control design to make data more valuable, wherein the cases and controls were matched for sex, age and T2DM duration. The study used conditional logistic regression analysis. These increased the accuracy in the estimation of the model. However, the shortcoming was the high risk of selection bias, as the samples were collected from hospitals. Although the risk factors for developing TB in patients with DM, and the epidemiological and pathobiological characteristics may be different in other regions of the world, the study by Shi et al[48] provides us with important risk factors for TB in T2DM cases that healthcare providers should be vigilant about at least in the Asian countries so that we can prevent or treat coexistent pulmonary TB in patients with T2DM.


The rising prevalence of DM worldwide is acknowledged as a resurgent risk factor and an obstacle to the control of TB. As each of these diseases perpetuates the risk and complications associated with one another, medical professionals should remain highly vigilant with the most up-to-date knowledge about TB and DM, and their co-existence in the same individual to optimise management strategies. More research on epidemiology, pathobiology, clinical characteristics, and diagnostic and therapeutic algorithms should enable improved disease care of this dangerous coexistence. The research data published by Shi et al[48], in the Journal is such an attempt to empower the global scientific fraternity.


We thank Dr. Marina George Kudiyirickal for providing the audio for the Core Tip of this paper.


Provenance and peer review: Invited article; Externally peer reviewed.

Peer-review model: Single blind

Specialty type: Endocrinology and metabolism

Country of origin: United Kingdom

Peer-review report’s classification

Scientific Quality: Grade B

Novelty: Grade B

Creativity or Innovation: Grade B

Scientific Significance: Grade B

P-Reviewer: Batta A, India S-Editor: Lin C L-Editor: A P-Editor: Zheng XM

1.  Bhargava A, Bhargava M, Meher A, Teja GS, Velayutham B, Watson B, Benedetti A, Barik G, Singh VP, Singh D, Madhukeshwar AK, Prasad R, Pathak RR, Chadha V, Joshi R. Nutritional support for adult patients with microbiologically confirmed pulmonary tuberculosis: outcomes in a programmatic cohort nested within the RATIONS trial in Jharkhand, India. Lancet Glob Health. 2023;11:e1402-e1411.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 18]  [Article Influence: 18.0]  [Reference Citation Analysis (0)]
2.  Ekramnia M, Li Y, Haddad MB, Marks SM, Kammerer JS, Swartwood NA, Cohen T, Miller JW, Horsburgh CR, Salomon JA, Menzies NA. Estimated rates of progression to tuberculosis disease for persons infected with Mycobacterium tuberculosis in the United States. Epidemiology. 2024;35:164-173.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
3.  World Health Organization  TB and diabetes. [cited 11 February 2024]. Available from: https://www.who.int/publications/digital/global-tuberculosis-report-2021/featured-topics/tb-diabetes.  [PubMed]  [DOI]  [Cited in This Article: ]
4.  Gautam S, Shrestha N, Mahato S, Nguyen TPA, Mishra SR, Berg-Beckhoff G. Diabetes among tuberculosis patients and its impact on tuberculosis treatment in South Asia: a systematic review and meta-analysis. Sci Rep. 2021;11:2113.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 47]  [Cited by in F6Publishing: 39]  [Article Influence: 13.0]  [Reference Citation Analysis (0)]
5.  Noubiap JJ, Nansseu JR, Nyaga UF, Nkeck JR, Endomba FT, Kaze AD, Agbor VN, Bigna JJ. Global prevalence of diabetes in active tuberculosis: a systematic review and meta-analysis of data from 2·3 million patients with tuberculosis. Lancet Glob Health. 2019;7:e448-e460.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 65]  [Cited by in F6Publishing: 53]  [Article Influence: 10.6]  [Reference Citation Analysis (0)]
6.  IDF Diabetes Atlas  IDF Diabetes Atlas 2021. [cited 11 February 2024]. Available from: https://diabetesatlas.org/atlas/tenth-edition/.  [PubMed]  [DOI]  [Cited in This Article: ]
7.  Ssekamatte P, Sande OJ, van Crevel R, Biraro IA. Immunologic, metabolic and genetic impact of diabetes on tuberculosis susceptibility. Front Immunol. 2023;14:1122255.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Reference Citation Analysis (0)]
8.  Berbudi A, Rahmadika N, Tjahjadi AI, Ruslami R. Type 2 Diabetes and its Impact on the Immune System. Curr Diabetes Rev. 2020;16:442-449.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 241]  [Cited by in F6Publishing: 380]  [Article Influence: 95.0]  [Reference Citation Analysis (0)]
9.  Martinez N, Ketheesan N, West K, Vallerskog T, Kornfeld H. Impaired Recognition of Mycobacterium tuberculosis by Alveolar Macrophages From Diabetic Mice. J Infect Dis. 2016;214:1629-1637.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 42]  [Cited by in F6Publishing: 47]  [Article Influence: 5.9]  [Reference Citation Analysis (0)]
10.  Kumar NP, Moideen K, Sivakumar S, Menon PA, Viswanathan V, Kornfeld H, Babu S. Modulation of dendritic cell and monocyte subsets in tuberculosis-diabetes co-morbidity upon standard tuberculosis treatment. Tuberculosis (Edinb). 2016;101:191-200.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 9]  [Cited by in F6Publishing: 10]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
11.  Krupa A, Fol M, Dziadek BR, Kepka E, Wojciechowska D, Brzostek A, Torzewska A, Dziadek J, Baughman RP, Griffith D, Kurdowska AK. Binding of CXCL8/IL-8 to Mycobacterium tuberculosis Modulates the Innate Immune Response. Mediators Inflamm. 2015;2015:124762.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 41]  [Cited by in F6Publishing: 47]  [Article Influence: 5.2]  [Reference Citation Analysis (0)]
12.  Chao WC, Yen CL, Wu YH, Chen SY, Hsieh CY, Chang TC, Ou HY, Shieh CC. Increased resistin may suppress reactive oxygen species production and inflammasome activation in type 2 diabetic patients with pulmonary tuberculosis infection. Microbes Infect. 2015;17:195-204.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 27]  [Cited by in F6Publishing: 30]  [Article Influence: 3.3]  [Reference Citation Analysis (0)]
13.  Tripathi D, Radhakrishnan RK, Thandi RS, Paidipally P, Devalraju KP, Neela VSK, McAllister MK, Samten B, Valluri VL, Vankayalapati R. Correction: IL-22 produced by type 3 innate lymphoid cells (ILC3s) reduces the mortality of type 2 diabetes mellitus (T2DM) mice infected with Mycobacterium tuberculosis. PLoS Pathog. 2021;17:e1009578.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 2]  [Article Influence: 0.7]  [Reference Citation Analysis (0)]
14.  Cheekatla SS, Tripathi D, Venkatasubramanian S, Nathella PK, Paidipally P, Ishibashi M, Welch E, Tvinnereim AR, Ikebe M, Valluri VL, Babu S, Kornfeld H, Vankayalapati R. NK-CD11c+ Cell Crosstalk in Diabetes Enhances IL-6-Mediated Inflammation during Mycobacterium tuberculosis Infection. PLoS Pathog. 2016;12:e1005972.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 24]  [Cited by in F6Publishing: 29]  [Article Influence: 3.6]  [Reference Citation Analysis (0)]
15.  Wang X, Ma A, Han X, Chan L, Liang H, Litifu A, Xue F. T Cell Profile was Altered in Pulmonary Tuberculosis Patients with Type 2 Diabetes. Med Sci Monit. 2018;24:636-642.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 7]  [Article Influence: 1.2]  [Reference Citation Analysis (0)]
16.  Kumar NP, Sridhar R, Banurekha VV, Jawahar MS, Nutman TB, Babu S. Expansion of pathogen-specific T-helper 1 and T-helper 17 cells in pulmonary tuberculosis with coincident type 2 diabetes mellitus. J Infect Dis. 2013;208:739-748.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 72]  [Cited by in F6Publishing: 80]  [Article Influence: 7.3]  [Reference Citation Analysis (0)]
17.  Meenakshi P, Ramya S, Lavanya J, Vijayalakshmi V, Sumanlatha G. Effect of IFN-γ, IL-12 and IL-10 cytokine production and mRNA expression in tuberculosis patients with diabetes mellitus and their household contacts. Cytokine. 2016;81:127-136.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 11]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
18.  Liu X, Li F, Niu H, Ma L, Chen J, Zhang Y, Peng L, Gan C, Ma X, Zhu B. IL-2 Restores T-Cell Dysfunction Induced by Persistent Mycobacterium tuberculosis Antigen Stimulation. Front Immunol. 2019;10:2350.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 16]  [Cited by in F6Publishing: 30]  [Article Influence: 6.0]  [Reference Citation Analysis (0)]
19.  Lyadova IV, Panteleev AV. Th1 and Th17 Cells in Tuberculosis: Protection, Pathology, and Biomarkers. Mediators Inflamm. 2015;2015:854507.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 128]  [Cited by in F6Publishing: 175]  [Article Influence: 19.4]  [Reference Citation Analysis (0)]
20.  Ayelign B, Negash M, Genetu M, Wondmagegn T, Shibabaw T. Immunological Impacts of Diabetes on the Susceptibility of Mycobacterium tuberculosis. J Immunol Res. 2019;2019:6196532.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 52]  [Cited by in F6Publishing: 81]  [Article Influence: 16.2]  [Reference Citation Analysis (0)]
21.  Bisht MK, Dahiya P, Ghosh S, Mukhopadhyay S. The cause-effect relation of tuberculosis on incidence of diabetes mellitus. Front Cell Infect Microbiol. 2023;13:1134036.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 3]  [Reference Citation Analysis (0)]
22.  Menon S, Rossi R, Dusabimana A, Zdraveska N, Bhattacharyya S, Francis J. The epidemiology of tuberculosis-associated hyperglycemia in individuals newly screened for type 2 diabetes mellitus: systematic review and meta-analysis. BMC Infect Dis. 2020;20:937.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 13]  [Article Influence: 3.3]  [Reference Citation Analysis (0)]
23.  Krishnappa D, Sharma SK, Singh AD, Sinha S, Ammini AC, Soneja M. Impact of tuberculosis on glycaemic status: A neglected association. Indian J Med Res. 2019;149:384-388.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 7]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
24.  Jiménez-Corona ME, Cruz-Hervert LP, García-García L, Ferreyra-Reyes L, Delgado-Sánchez G, Bobadilla-Del-Valle M, Canizales-Quintero S, Ferreira-Guerrero E, Báez-Saldaña R, Téllez-Vázquez N, Montero-Campos R, Mongua-Rodriguez N, Martínez-Gamboa RA, Sifuentes-Osornio J, Ponce-de-León A. Association of diabetes and tuberculosis: impact on treatment and post-treatment outcomes. Thorax. 2013;68:214-220.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 158]  [Cited by in F6Publishing: 194]  [Article Influence: 16.2]  [Reference Citation Analysis (0)]
25.  Dolasia K, Bisht MK, Pradhan G, Udgata A, Mukhopadhyay S. TLRs/NLRs: Shaping the landscape of host immunity. Int Rev Immunol. 2018;37:3-19.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 77]  [Cited by in F6Publishing: 82]  [Article Influence: 11.7]  [Reference Citation Analysis (0)]
26.  Bhat KH, Chaitanya CK, Parveen N, Varman R, Ghosh S, Mukhopadhyay S. Proline-proline-glutamic acid (PPE) protein Rv1168c of Mycobacterium tuberculosis augments transcription from HIV-1 Long terminal repeat promoter. J Biol Chem. 2012;287:16930-16946.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 25]  [Cited by in F6Publishing: 27]  [Article Influence: 2.3]  [Reference Citation Analysis (0)]
27.  Parveen N, Varman R, Nair S, Das G, Ghosh S, Mukhopadhyay S. Endocytosis of Mycobacterium tuberculosis heat shock protein 60 is required to induce interleukin-10 production in macrophages. J Biol Chem. 2013;288:24956-24971.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 35]  [Cited by in F6Publishing: 36]  [Article Influence: 3.3]  [Reference Citation Analysis (0)]
28.  Xu G, Jia H, Li Y, Liu X, Li M, Wang Y. Hemolytic phospholipase Rv0183 of Mycobacterium tuberculosis induces inflammatory response and apoptosis in alveolar macrophage RAW264.7 cells. Can J Microbiol. 2010;56:916-924.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 16]  [Cited by in F6Publishing: 17]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
29.  Wang L, Liu Z, Wang J, Liu H, Wu J, Tang T, Li H, Yang H, Qin L, Ma D, Chen J, Liu F, Wang P, Zheng R, Song P, Zhou Y, Cui Z, Wu X, Huang X, Liang H, Zhang S, Cao J, Wu C, Chen Y, Su D, Chen X, Zeng G, Ge B. Oxidization of TGFβ-activated kinase by MPT53 is required for immunity to Mycobacterium tuberculosis. Nat Microbiol. 2019;4:1378-1388.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 15]  [Cited by in F6Publishing: 17]  [Article Influence: 3.4]  [Reference Citation Analysis (0)]
30.  Quiding-Järbrink M, Smith DA, Bancroft GJ. Production of matrix metalloproteinases in response to mycobacterial infection. Infect Immun. 2001;69:5661-5670.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 109]  [Cited by in F6Publishing: 107]  [Article Influence: 4.7]  [Reference Citation Analysis (0)]
31.  Chen N, Zhou L, Zhang Z, Xu J, Wan Z, Qin L. Resistin induces lipolysis and suppresses adiponectin secretion in cultured human visceral adipose tissue. Regul Pept. 2014;194-195:49-54.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 18]  [Cited by in F6Publishing: 18]  [Article Influence: 1.8]  [Reference Citation Analysis (0)]
32.  Zhang HH, Halbleib M, Ahmad F, Manganiello VC, Greenberg AS. Tumor necrosis factor-alpha stimulates lipolysis in differentiated human adipocytes through activation of extracellular signal-related kinase and elevation of intracellular cAMP. Diabetes. 2002;51:2929-2935.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 312]  [Cited by in F6Publishing: 301]  [Article Influence: 13.7]  [Reference Citation Analysis (0)]
33.  Martinez N, Cheng CY, Ketheesan N, Cullen A, Tang Y, Lum J, West K, Poidinger M, Guertin DA, Singhal A, Kornfeld H. mTORC2/Akt activation in adipocytes is required for adipose tissue inflammation in tuberculosis. EBioMedicine. 2019;45:314-327.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 9]  [Article Influence: 1.8]  [Reference Citation Analysis (0)]
34.  Oswal N, Lizardo K, Dhanyalayam D, Ayyappan JP, Thangavel H, Heysell SK, Nagajyothi JF. Host Metabolic Changes during Mycobacterium Tuberculosis Infection Cause Insulin Resistance in Adult Mice. J Clin Med. 2022;11.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 9]  [Article Influence: 4.5]  [Reference Citation Analysis (0)]
35.  Ordway D, Henao-Tamayo M, Orme IM, Gonzalez-Juarrero M. Foamy macrophages within lung granulomas of mice infected with Mycobacterium tuberculosis express molecules characteristic of dendritic cells and antiapoptotic markers of the TNF receptor-associated factor family. J Immunol. 2005;175:3873-3881.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 80]  [Cited by in F6Publishing: 81]  [Article Influence: 4.3]  [Reference Citation Analysis (0)]
36.  Howard NC, Khader SA. Immunometabolism during Mycobacterium tuberculosis Infection. Trends Microbiol. 2020;28:832-850.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 20]  [Cited by in F6Publishing: 34]  [Article Influence: 8.5]  [Reference Citation Analysis (0)]
37.  Lin H, Xing J, Wang H, Wang S, Fang R, Li X, Li Z, Song N. Roles of Lipolytic enzymes in Mycobacterium tuberculosis pathogenesis. Front Microbiol. 2024;15:1329715.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
38.  Singh V, Kaur C, Chaudhary VK, Rao KV, Chatterjee S. M. tuberculosis Secretory Protein ESAT-6 Induces Metabolic Flux Perturbations to Drive Foamy Macrophage Differentiation. Sci Rep. 2015;5:12906.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 35]  [Cited by in F6Publishing: 37]  [Article Influence: 4.1]  [Reference Citation Analysis (0)]
39.  Zhan S, Juan X, Ren T, Wang Y, Fu L, Deng G, Zhang P. Extensive Radiological Manifestation in Patients with Diabetes and Pulmonary Tuberculosis: A Cross-Sectional Study. Ther Clin Risk Manag. 2022;18:595-602.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 4]  [Article Influence: 2.0]  [Reference Citation Analysis (0)]
40.  Ruesen C, Chaidir L, Ugarte-Gil C, van Ingen J, Critchley JA, Hill PC, Ruslami R, Santoso P, Huynen MA, Dockrell HM, Moore DAJ, Alisjahbana B, van Crevel R. Diabetes is associated with genotypically drug-resistant tuberculosis. Eur Respir J. 2020;55.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 5]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
41.  Elshamly M, Nour MO, Omar AMM. Clinical presentations and outcome of severe community-acquired pneumonia. Egypt J Chest Dis Tuberc. 2016;65:831-839.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 6]  [Article Influence: 0.8]  [Reference Citation Analysis (0)]
42.  Tegegne BS, Mengesha MM, Teferra AA, Awoke MA, Habtewold TD. Association between diabetes mellitus and multi-drug-resistant tuberculosis: evidence from a systematic review and meta-analysis. Syst Rev. 2018;7:161.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 37]  [Cited by in F6Publishing: 47]  [Article Influence: 7.8]  [Reference Citation Analysis (0)]
43.  Huangfu P, Ugarte-Gil C, Golub J, Pearson F, Critchley J. The effects of diabetes on tuberculosis treatment outcomes: an updated systematic review and meta-analysis. Int J Tuberc Lung Dis. 2019;23:783-796.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 47]  [Cited by in F6Publishing: 51]  [Article Influence: 10.2]  [Reference Citation Analysis (0)]
44.  Song C, Xie W, Gong L, Ren M, Pan P, Luo B. The relationship between HbA1c control levels and antituberculosis treatment effects: a meta-analysis. J Chin Med Assoc. 2019;82:915-921.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 5]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
45.  Kornfeld H, Procter-Gray E, Kumpatla S, Kane K, Li W, Magee MJ, Babu S, Viswanathan V. Longitudinal trends in glycated hemoglobin during and after tuberculosis treatment. Diabetes Res Clin Pract. 2023;196:110242.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
46.  Yorke E, Atiase Y, Akpalu J, Sarfo-Kantanka O, Boima V, Dey ID. The Bidirectional Relationship between Tuberculosis and Diabetes. Tuberc Res Treat. 2017;2017:1702578.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 20]  [Cited by in F6Publishing: 26]  [Article Influence: 3.7]  [Reference Citation Analysis (0)]
47.  Schutz C, Davis AG, Sossen B, Lai RP, Ntsekhe M, Harley YX, Wilkinson RJ. Corticosteroids as an adjunct to tuberculosis therapy. Expert Rev Respir Med. 2018;12:881-891.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 37]  [Cited by in F6Publishing: 30]  [Article Influence: 5.0]  [Reference Citation Analysis (0)]
48.  Shi H, Yuan Y, Li X, Li YF, Fan L, Yang XM. Analysis of the influencing factors and clinical related characteristics of pulmonary tuberculosis in patients with type 2 diabetes mellitus. World J Diabetes. 2024;15:196-208.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]