| dc.description.abstract | Background: Mycobacterium tuberculosis (Mtb) remains a successful pathogen causing tuberculosis (TB), and the burden of TB disease is constantly increasing. Although great progress has been made in delineating the disease, the host-pathogen interactions are incompletely understood. Individuals with diabetes mellitus have been shown to have an increased risk of acquiring (Mtb) infection and disease. However, the underlying mechanisms associated with this susceptibility are not well established. Interleukin (IL)-35 is a relatively newly discovered unique member of the IL-12 cytokine family. Recent studies show that IL35 is expressed highly in DM or TB patients. The role of the new subpopulation of this regulatory cytokine in DM and TB is not known. This project proposes to evaluate the level of this cytokine and its role in increasing the risk of TB among diabetic patients. Besides, the levels of this new cytokine would be compared to other cytokines, in trying to understand the pathoimmunology of DM in TB.
Methods: This project used stored whole blood culture supernatants from the QuantiferonGold plus assay (QFT) assay analysed in the TB and Diabetes (TAD) study. The supernatants were thawed, and Luminex and ELISA assays were used to determine the different levels of IL-35 and other cytokines. Data were managed and manipulated in Microsoft excel sheet and thereafter exported to Graph pad version 8 for analysis and generation of graphs.
Results: Among the 136 patients in this study, 40 had DM and LTBI, 17 DM only, 39 LTBI only, and 44 uninfected healthy individuals. The IL-35 levels was more elevated in the patients with both DM and LTBI than in all other groups (median (0.1837), P-v (0.012)), while IL-10 concentrations were highest among the LTBI only group (median (0.00221); p-valve (0.0125)). IFN-γ, a Th1 cytokine which plays a significant role in TB protection was highly elevated in patients with DM and LTBI (median (0.9211); p-valve (0.003)). There were no statistically supported differences for the rest of the cytokines (TNF, IL-4, IL-13, IL-17, IL-21, and IL-22) among the study groups.
Conclusion: Higher production of IL-35 was detected in patients with both DM and LTBI than in patients with DM, LTBI, or healthy individuals only, suggesting a likely inhibitory role of IL-35 as has been demonstrated in other studies. IFN-g, a Th1 cytokine which plays a big role in TB protection was highly elevated in patient with DM and LTBI, suggesting that LTBI was immune modulating the production of IFN-g. We suggest that the role of IL-35 should be further evaluated and confirmed in future research, especially cohort studies. | en_US |
