4.2 Article

Neutrophils from pulmonary tuberculosis patients show augmented levels of chemokines MIP-1α, IL-8 and MCP-1 which further increase upon in vitro infection with mycobacterial strains

Journal

HUMAN IMMUNOLOGY
Volume 75, Issue 8, Pages 914-922

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.humimm.2014.06.020

Keywords

Neutrophil; Mycobacterium; H37Rv; Chemokine; Chemokine receptor

Categories

Funding

  1. UGC

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Neutrophils being innate cells initiate the immune defence against mycobacteria by sending signals to other immune cells. Chemokines being the vital link in signaling processes, it is of interest to study their secretion by neutrophils as a response to tuberculosis infection. The levels of various chemokines (MIP-1 alpha, MCP-1, IL-8 and IP-10) and chemokine receptors (CXCR1, CXCR2 and CCR1) in neutrophils from healthy individuals and pulmonary tuberculosis patients were studied following infection with Mycobacterium tuberculosis strains (clinical - S7 and S10 and laboratory - H37Rv). The release of MIP-1 alpha, IL-8 and MCP-1 is found to be greatly increased in patient neutrophils. Mycobacterial strains differentially influenced neutrophils affecting the release of chemokines to different extent. H37Rv significantly increased the release of MIP-1 alpha and IL-8 in both normals and tuberculosis patients, while S10 up regulated only the release of MIP-1 alpha in patients. Thus, during tuberculosis, neutrophils undergo functional alteration to combat infection. While H37Rv is greatly recognized by neutrophils and triggers the release of chemokines, clinical strains by some means try to suppress immune activation of neutrophils in their favor. (C) 2014 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.

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