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PPE2 protein of Mycobacterium tuberculosis may inhibit nitric oxide in activated macrophages
Author(s) -
Bhat Khalid Hussain,
Das Arghya,
Srikantam Aparna,
Mukhopadhyay Sangita
Publication year - 2013
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.12070
Subject(s) - nitric oxide , mycobacterium tuberculosis , pathogenesis , microbiology and biotechnology , tuberculosis , pathogen , bacilli , mycobacterium , human pathogen , bacteria , biology , immunology , chemistry , medicine , pathology , genetics , endocrinology
Although the pathophysiological role of PE/PPE proteins of Mycobacterium tuberculosis is yet to be fully understood, recent evidence shows that these proteins play important roles in antigenic diversity, as well as in host–pathogen interactions and mycobacterial pathogenesis. Most of the PE/PPE proteins are highly expressed in pathogenic bacteria, pointing to their role in the pathogenesis of mycobacteria. Here, we provide an overview of our work in progress on a specific PPE protein, PPE2 (Rv0256c), which may inhibit nitric oxide (NO) production in activated macrophages. As NO and its by‐products are considered to be toxic to bacilli, it is possible that the bacilli recruit Rv0256c in order to inhibit higher production of NO during infection.