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Kim and Shin: Apoptotic Effect of Macrophages against Mycobacterium tuberculosis
Research Update (Minireview)

J Bacteriol Virol 2016;46(4):312-318.

Published online: 9 February 2016

DOI: https://doi.org/10.4167/jbv.2016.46.4.312

Apoptotic Effect of Macrophages against Mycobacterium tuberculosis

Lee-Han Kim, Sung Jae Shin∗

Department of Microbiology, Institute of Immunology and Immunological Diseases, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea

∗Corresponding author: Sung Jae Shin. Department of Microbiology and Institute of Immunology and Immunological Diseases, Yonsei University College of Medicine, 50 Yonsei-ro, Seodaemun-gu, Seoul 03722, Korea. Phone: +82-2-2228-1813, Fax: +82-2-392-9310, e-mail: sjshin@yuhs.ac

∗∗ This study was supported by the Basic Science Research Program and the International Research & Development Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT & Future Planning of Korea (NRF-2016R1A2A1A05005263 and NRF-2014K1A3A7A03075054).

Received 9 December 20169 December 2016       Accepted 9 December 2016

Copyright © 2016 Journal of Bacteriology and Virology

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Mycobacterium tuberculosis (Mtb) causing tuberculosis as an intracellular pathogen initially infects alveolar macrophages following aerosol inhalation. Thus, macrophages play a critical role in the establishment of Mtb infection and macrophage cell death, a common outcome during Mtb infection, may initiate host- or pathogen-favored immune responses, resulting in facilitating protection or pathogenesis, respectively. In addition, virulent Mtb strains are known to inhibit apoptosis and consequently down-regulates immune response using a variety of strategies. In many recent studies have shown that virulent Mtb can either augment or reduce apoptosis by regulating expression of pro-apoptotic and anti-apoptotic proteins belonging to Bcl-2 family proteins. In this review, we will discuss and dissect the apoptotic pathways of Bcl-2 family proteins in Mtb-infected macrophages.

Keywords: Mycobacterium tuberculosis, Apoptosis, Bcl-2 family proteins, Anti-apoptotic proteins, Pro-apoptotic proteins

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Figure 1.
Regulation of apoptosis signaling pathway by Bcl-2 family proteins. The mitochondrial outer membrane permeabilization (MOMP) can be regulated by either extrinsic (death receptor-mediated) and intrinsic (mitochondria-mediated) pathways. MOMP triggers the release of apoptogenic factor such as cytochrome c into cytosol to facilitate activation of caspase 3, resulting in induction of apoptosis. Virulent Mtb promotes the induction and production of Bcl-2 family proteins (①) and eventually inhibits apoptosis pathways (②) to multiplicate inside macrophages. FADD; Fas-associated death domain, Bax; Bcl-2-associated X protein, Bak; Bcl-2-antagonist killer, (t)Bid;(truncated) Bax-like BH3 protein, DISC; Death inducing signaling complex, Apaf1; Apoptotic protease activating factor 1, Mtb; Mycobacterium tuberculosis
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