Protein kinase E of Mycobacterium tuberculosis has a role in the nitric oxide stress response and apoptosis in a human macrophage model of infection

Deepak, Jayakumar and Jacob, W R and Sujatha, Narayanan (2008) Protein kinase E of Mycobacterium tuberculosis has a role in the nitric oxide stress response and apoptosis in a human macrophage model of infection. Cellular Microbiology, 10 (2). pp. 365-374. ISSN Online: 1462-5822

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Abstract

Mycobacterium tuberculosis, an intracellular pathogen, inhibits macrophage apoptosis to support survival and replication inside the host cell. We provide evidence that the functional serine/threonine kinase, PknE, is important for survival of M. tuberculosis that enhances macrophage viability by inhibiting apoptosis.Apromoter of PknE identified in this study was shown to respond to nitric oxide stress. Deletion of pknE in virulent M. tuberculosis, H37Rv, resulted in a strain that has increased resistance to nitric oxide donors and increased sensitivity to reducing agents. The deletion mutant created by specialized transduction induced enhanced apoptosis while inhibiting necrosis. The pknE mutant also modifies the innate immune response as shown by the marked decline in the pro-inflammatory cytokines in a macrophage model of infection. These findings suggest a novel mechanism,bywhichPknEsensesnitricoxidestress and prevents apoptosis by interfering with host signalling pathways.

Item Type:	Article
Additional Information:	doi:10.1111/j.1462-5822.2007.01049.x
Subjects:	Tuberculosis > Laboratory Research Tuberculosis > Laboratory Research > Immunological Tuberculosis
Divisions:	Basic Science Research > Immunology
Depositing User:	Dr. Rathinasabapati R
Date Deposited:	31 May 2017 07:48
Last Modified:	24 Mar 2021 08:59
URI:	http://eprints.nirt.res.in/id/eprint/866

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