Mycobacterium tuberculosis: prePPARing and Maintaining the Replicative Niche

Michael D Stutz; Marc Pellegrini

doi:10.1016/j.tim.2018.08.001

Mycobacterium tuberculosis: prePPARing and Maintaining the Replicative Niche

Trends Microbiol. 2018 Oct;26(10):813-814. doi: 10.1016/j.tim.2018.08.001. Epub 2018 Aug 14.

Authors

Michael D Stutz¹, Marc Pellegrini²

Affiliations

¹ Infection and Immunity Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia; Department of Medical Biology, The University of Melbourne, Melbourne, VIC, Australia.
² Infection and Immunity Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia; Department of Medical Biology, The University of Melbourne, Melbourne, VIC, Australia. Electronic address: pellegrini@wehi.edu.au.

PMID: 30119946
DOI: 10.1016/j.tim.2018.08.001

Abstract

Mycobacterium tuberculosis interferes with the ability of its host cell to undergo apoptosis. Arnett et al. report that the pathogen promotes macrophage survival by engaging the nuclear receptor PPARγ to induce the antiapoptotic protein MCL-1, yielding insights into the pathogenesis of tuberculosis and potentially unlocking new avenues for therapeutic intervention.

Keywords: MCL-1; PPARγ; apoptosis; host-directed therapy; tuberculosis.

Publication types

Research Support, Non-U.S. Gov't
Comment

MeSH terms

Apoptosis
Humans
Macrophages
Mycobacterium tuberculosis*
Myeloid Cell Leukemia Sequence 1 Protein
PPAR gamma
Tuberculosis*

Substances

Myeloid Cell Leukemia Sequence 1 Protein
PPAR gamma