Tuberculosis and the art of macrophage manipulation

被引:109
|
作者
Upadhyay, S. [1 ]
Mittal, E. [1 ]
Philips, J. A. [1 ]
机构
[1] Washington Univ, Sch Med, Div Infect Dis, Dept Med,Dept Mol Microbiol, St Louis, MO 63110 USA
来源
PATHOGENS AND DISEASE | 2018年 / 76卷 / 04期
基金
美国国家卫生研究院;
关键词
tuberculosis; phagosome maturation; LC3-associated phagocytosis; autophagy; apoptosis; inflammasome; PHAGOSOME MATURATION ARREST; INTRACELLULAR MYCOBACTERIUM-TUBERCULOSIS; TYROSINE-PHOSPHATASE PTPA; BACILLUS-CALMETTE-GUERIN; ESX-1 SECRETION SYSTEM; PROTEIN-KINASE-G; INFECTED MACROPHAGES; ALVEOLAR MACROPHAGES; NLRP3; INFLAMMASOME; NADPH OXIDASE;
D O I
10.1093/femspd/fty037
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Macrophages are first-line responders against microbes. The success of Mycobacterium tuberculosis (Mtb) rests upon its ability to convert these antimicrobial cells into a permissive cellular niche. This is a remarkable accomplishment, as the antimicrobial arsenal of macrophages is extensive. Normally bacteria are delivered to an acidic, degradative lysosome through one of several trafficking pathways, including LC3-associated phagocytosis (LAP) and autophagy. Once phagocytozed, the bacilli are subjected to reactive oxygen and nitrogen species, and they induce the expression of proinflammatory cytokines, which serve to augment host responses. However, Mtb hijacks these host defense mechanisms, manipulating host cellular trafficking, innate immune responses, and cell death pathways to its benefit. The complex series of measures and countermeasures between host and pathogen ultimately determines the outcome of infection. In this review, we focus on the diverse effectors that Mtb uses in its multipronged effort to subvert the innate immune responses of macrophages. We highlight recent advances in understanding the molecular interface of the Mtb-macrophage interaction.
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页数:12
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