Type 2 diabetes mellitus coincident with pulmonary or latent tuberculosis results in modulation of adipocytokines

Kumar, Nathella Pavan; Nair, Dina; Velayutham, Banurekha; Dolla, Chandrakumar; Kumaran, Paul; Ramaswamy, Sridhar; Babu, Subash

doi:10.1016/j.cyto.2015.12.026

Cited by 26 publications

(21 citation statements)

References 42 publications

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“…In our published studies, we found that except for IL-22, all pro- and anti-inflammatory cytokine levels (Th1, Th2 and Th17) were significantly higher in the lungs of Mtb -infected T2DM mice than in the lungs of nondiabetic Mtb -infected mice [19]. Similar findings were noted in the plasma of T2DM TB patients compared with that of TB patients without T2DM [26,55]. Our current findings confirm these findings and further demonstrate that ILC3s are an important source of IL-22 in Mtb -infected mouse lungs, and defective IL-22 production by ILC3s in T2DM mice infected with Mtb leads to epithelial cell damage and enhanced mortality.…”

Section: Discussionmentioning

confidence: 56%

IL-22 produced by type 3 innate lymphoid cells (ILC3s) reduces the mortality of type 2 diabetes mellitus (T2DM) mice infected with Mycobacterium tuberculosis

et al. 2019

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Previously, we found that pathological immune responses enhance the mortality rate of Mycobacterium tuberculosis (Mtb)-infected mice with type 2 diabetes mellitus (T2DM). In the current study, we evaluated the role of the cytokine IL-22 (known to play a protective role in bacterial infections) and type 3 innate lymphoid cells (ILC3s) in regulating inflammation and mortality in Mtb-infected T2DM mice. IL-22 levels were significantly lower in Mtb-infected T2DM mice than in nondiabetic Mtb-infected mice. Similarly, serum IL-22 levels were significantly lower in tuberculosis (TB) patients with T2DM than in TB patients without T2DM. ILC3s were an important source of IL-22 in mice infected with Mtb, and recombinant IL-22 treatment or adoptive transfer of ILC3s prolonged the survival of Mtb-infected T2DM mice. Recombinant IL-22 treatment reduced serum insulin levels and improved lipid metabolism. Recombinant IL-22 treatment or ILC3 transfer prevented neutrophil accumulation near alveoli, inhibited neutrophil elastase 2 (ELA2) production and prevented epithelial cell damage, identifying a novel mechanism for IL-22 and ILC3-mediated inhibition of inflammation in T2DM mice infected with an intracellular pathogen. Our findings suggest that the IL-22 pathway may be a novel target for therapeutic intervention in T2DM patients with active TB disease.

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Section: Discussionmentioning

confidence: 56%

IL-22 produced by type 3 innate lymphoid cells (ILC3s) reduces the mortality of type 2 diabetes mellitus (T2DM) mice infected with Mycobacterium tuberculosis

et al. 2019

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“…This possibly happens through the activities of adipocytokines—cytokines produced by the adipose tissues of T2DM patients. Adipokines induce inflammatory processes in patients with T2DM and dysregulation of this cytokine has an impact on increased risk of developing LTBI in patients with T2DM [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

Prevalence and Risk Factors of Latent Tuberculosis Infection (LTBI) in Patients with Type 2 Diabetes Mellitus (T2DM)

Ping

Zakaria

Islam

et al. 2021

IJERPH

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Type 2 diabetes mellitus (T2DM) and tuberculosis (TB) together impose a high disease burden in terms of both mortality and health economics worldwide. The objective of this study was to estimate the prevalence and risk factors of latent TB infection (LTBI) in patients with T2DM in Malaysia. A cross-sectional study was performed, and adult T2DM patients (n = 299) were included. Simple and multiple logistic regression analyses were performed to identify the LTBI-associated risk factors in patients with T2DM. Multiple logistic regression was used to estimate adjusted odds ratios (aOR) and 95% confidence intervals (CIs) between T2DM and LTBI and was adjusted for potential confounders. The prevalence of LTBI in patients with T2DM was 11.4% (95% CI: 8.0–15.0%). There was no significant difference in the socio-demographic characteristics between LTBI and non-LTBI subjects. No significant difference in the smoking status, the duration of smoking, and the duration of T2DM, HbA1c, or treatments was observed. Interestingly, a higher level of education was observed to be associated with a lower prevalence of LTBI in T2DM patients (aOR: 0.08, 95% CI: 0.01–0.70, p = 0.02). Although the prevalence of LTBI in T2DM was low, it is important to screen for it in T2DM patients due to the risk of developing severe active TB.

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“…Adipose tissue is a central inflammatory source in obesity and type 2 DM, not only because of cytokines produced from the adipocyte itself, but also because of infiltration by pro‐inflammatory macrophages . To study the influence of DM on active PTB and LTB, Kumar et al . examined circulating levels of adipocytokines in the plasma of individuals with PTB‐DM or LTB‐DM and compared them with those without DM (PTB or LTB).…”

Section: Biomarkers Associated With Tb‐dm Co‐morbiditymentioning

confidence: 99%

“…In addition, adiponectin and adipsin display a significant negative correlation, whereas leptin, visfatin and plasminogen activator inhibitor‐1 (PAI‐1) show a significant positive correlation with HbA1C levels and random blood glucose levels. The authors suggest that alterations in the systemic levels of adipocytokines indicate that altered adipose tissue inflammation underlying type 2 DM potentially contributes to the pathogenesis of TB disease …”

Section: Biomarkers Associated With Tb‐dm Co‐morbiditymentioning

confidence: 99%

Influence of diabetes mellitus on immunity to human tuberculosis

2017

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SummaryType 2 diabetes mellitus(DM) is a major risk factor for the development of active pulmonary tuberculosis (TB), with development of DM pandemic in countries where TB is also endemic. Understanding the impact of DM on TB and the determinants of co-morbidity is essential in responding to this growing public health problem with improved therapeutic approaches. Despite the clinical and public health significance posed by the dual burden of TB and DM, little is known about the immunological and biochemical mechanisms of susceptibility. One possible mechanism is that an impaired immune response in patients with DM facilitates either primary infection with Mycobacterium tuberculosis or reactivation of latent TB. Diabetes is associated with immune dysfunction and alterations in the components of the immune system, including altered levels of specific cytokines and chemokines. Some effects of DM on adaptive immunity that are potentially relevant to TB defence have been identified in humans. In this review, we summarize current findings regarding the alterations in the innate and adaptive immune responses and immunological mechanisms of susceptibility of patients with DM to M. tuberculosis infection and disease.

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Type 2 diabetes mellitus coincident with pulmonary or latent tuberculosis results in modulation of adipocytokines

Cited by 26 publications

References 42 publications

IL-22 produced by type 3 innate lymphoid cells (ILC3s) reduces the mortality of type 2 diabetes mellitus (T2DM) mice infected with Mycobacterium tuberculosis

IL-22 produced by type 3 innate lymphoid cells (ILC3s) reduces the mortality of type 2 diabetes mellitus (T2DM) mice infected with Mycobacterium tuberculosis

Prevalence and Risk Factors of Latent Tuberculosis Infection (LTBI) in Patients with Type 2 Diabetes Mellitus (T2DM)

Influence of diabetes mellitus on immunity to human tuberculosis

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