Display options
Cite
Masood KI, Irfan M, Masood Q, et al. Latent M. tuberculosis infection is associated with increased inflammatory cytokine and decreased Suppressor of cytokine signaling (SOCS)-3 in the diabetic host. Scand J Immunol. 2021;e13134doi: 10.1111/sji.13134.
Masood, K. I., Irfan, M., Masood, Q., Yameen, M., Jamil, B., Ram, N., Rao, S., Rottenberg, M., & Hasan, Z. (2021). Latent M. tuberculosis infection is associated with increased inflammatory cytokine and decreased Suppressor of cytokine signaling (SOCS)-3 in the diabetic host. Scandinavian journal of immunology, e13134. https://doi.org/10.1111/sji.13134
Masood, Kiran Iqbal, et al. "Latent M. tuberculosis infection is associated with increased inflammatory cytokine and decreased Suppressor of cytokine signaling (SOCS)-3 in the diabetic host." Scandinavian journal of immunology vol. (2021): e13134. doi: https://doi.org/10.1111/sji.13134
Masood KI, Irfan M, Masood Q, Yameen M, Jamil B, Ram N, Rao S, Rottenberg M, Hasan Z. Latent M. tuberculosis infection is associated with increased inflammatory cytokine and decreased Suppressor of cytokine signaling (SOCS)-3 in the diabetic host. Scand J Immunol. 2021 Dec 24;e13134. doi: 10.1111/sji.13134. Epub 2021 Dec 24. PMID: 34951048.
Copy Download .nbib Format: NLM
Share it on

Scand J Immunol. 2021 Dec 24;e13134. doi: 10.1111/sji.13134. Epub 2021 Dec 24.

Latent M. tuberculosis infection is associated with increased inflammatory cytokine and decreased Suppressor of cytokine signaling (SOCS)-3 in the diabetic host.

Scandinavian journal of immunology

Kiran Iqbal Masood, Muhammad Irfan, Qamar Masood, Maliha Yameen, Bushra Jamil, Nanik Ram, Shoaib Rao, Martin Rottenberg, Zahra Hasan

Affiliations

  1. Department of Pathology and Laboratory Medicine, The Aga Khan University Karachi, Pakistan; Department of Medicine, The Aga Khan University Karachi, Pakistan; Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Sweden.

PMID: 34951048 DOI: 10.1111/sji.13134

Abstract

Tuberculosis (TB) outcomes are worsened by type II diabetes mellitus (DM). Protective immunity against Mycobacterium tuberculosis (MTB) is driven by cytokines. Latent TB (LTBi) is common but its effect on the diabetic host is not well understood. We investigated mycobacterial antigen stimulated responses in peripheral blood mononuclear cell (PBMC) isolated from healthy endemic controls (EC), those with LTBi, DM groups with and without LTBi, as compared with TB patients. Cytokines were measured using a Luminex based assay. Gene expression was determined by RT-PCR. In DM-LTBi cases, PPD-stimulated pro-inflammatory cytokines; IFN-γ, IL-6, IL-2, TNF-α and GM-CSF and anti-inflammatory cytokines, IL-5 and IL-13 were raised as compared with EC. DM-LTBi PPD-stimulated IFN-γ, IL-6 and TNF-α mRNA titers were found raised in DM-LTBi whilst, suppressor of cytokine signaling (SOCS)-3 expression was lowered. Within DM cases, stratification based on HbA1c levels revealed raised IFN-γ but lowered IL-6 gene expression in those with controlled levels as compared with uncontrolled glycemic levels. Further, SOCS1 expression levels were found higher in DM cases with controlled glycemia when compared with EC. Overall, we show that diabetics with LTBi manifest raised levels of inflammatory and anti-inflammatory cytokines concomitant with reduced SOCS3 mRNA expression. Reduced glycemic control results in further inflammatory dysregulation impacting conversing impacting IFN-γ and IL-6 activation. These results suggest that dysregulated immune activation in diabetes is exacerbated by LTBi, lack of glycemic control may further compromise immunity against MTB infection.

This article is protected by copyright. All rights reserved.

Keywords: IL-6; SOCS3; latent TB; type 2 diabetes

Publication Types