Elevated Unstimulated and TB Antigen Stimulated Levels of IL-36 Family of Cytokines In Pulmonary and Extra-pulmonary Tuberculosis


Identification: Nancy-Arul


Description

Elevated Unstimulated and TB Antigen Stimulated Levels of IL-36 Family of Cytokines In Pulmonary and Extra-pulmonary Tuberculosis
Authors: Arul Nancy 1, Nathella Pavan Kumar 2, Gokul Raj Kathamuthu 1,2, Kadar Moideen 1, Rathinam Sridhar,3 Dhanaraj Baskaran2 and Subash Babu 1,4
Affiliation: 1National Institutes of Health – NIRT - International Center for Excellence in Research, Chennai, India; 2National Institute for Research in Tuberculosis, Chennai, India; 3Government Stanley Medical Hospital, Chennai and 4LPD, NIAID, NIH, MD, USA.

Abstract
Background: The IL-36 subfamily comprises of the proinflammatory molecules, IL-36α, IL-36β, IL-36γ and the putative IL-36 receptor antagonist (IL-36Ra). Previous studies have reported that IL-36 production is triggered by Mycobacterium tuberculosis infection and that IL-36 plays a critical role in limiting bacterial growth. However, a detailed examination of the association of IL-36 family of cytokines in pulmonary TB (PTB) and extra-pulmonary TB (ETB) has not been done.
Methods and Objectives: To explore this, we examined the unstimulated as well as TB-antigen and mitogen stimulated levels of IL-36 isoforms in PTB, ETB, latent TB (LTB) and healthy individuals (Non-TB).
Results: PTB individuals exhibited a significantly increased unstimulated (NIL) and TB antigen stimulated net cytokine levels of IL-36α, IL-36γ and IL-36Ra in comparison to ETB, LTB and Non-TB individuals. In addition, ETB individuals also exhibited a significantly increased unstimulated (NIL) and TB antigen stimulated net cytokine levels of IL-36α, IL-36γ and IL-36Ra in comparison to LTB and Non-TB individuals. Finally, ETB individuals also exhibited a significantly increased unstimulated (NIL) and TB antigen stimulated net cytokine levels of IL-36b in comparison to PTB, LTB and NTB individuals.
Conclusion: Our data on IL-36 family of cytokines suggest that upregulation of these IL-1 superfamily cytokines and of their common receptor antagonist, might contribute to the hyperinflammatory immune pathology characteristic of pulmonary and extra-pulmonary TB disease. 

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