Contrasting Lifestyles Within the Host Cell

被引:25
作者
Case, Elizabeth Di Russo [1 ]
Samuel, James E. [1 ]
机构
[1] Texas A&M Hlth Sci Ctr, Coll Med, Dept Microbial Pathogenesis & Immunol, Bryan, TX 77807 USA
来源
MICROBIOLOGY SPECTRUM | 2016年 / 4卷 / 01期
关键词
MYCOBACTERIUM-TUBERCULOSIS PHAGOSOME; ENDOCYTIC MULTIVESICULAR BODIES; CU; ZN SUPEROXIDE-DISMUTASE; NITRIC-OXIDE SYNTHASE; COXIELLA-BURNETII; BRUCELLA-ABORTUS; CHLAMYDIAL INCLUSION; LYSOSOME FUSION; Q-FEVER; ALPHA(V)BETA(3) INTEGRIN;
D O I
10.1128/microbiolspec.VMBF-0014-2015
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Intracellular bacterial pathogens have evolved to exploit the protected niche provided within the boundaries of a eukaryotic host cell. Upon entering a host cell, some bacteria can evade the adaptive immune response of its host and replicate in a relatively nutrient-rich environment devoid of competition from other host flora. Growth within a host cell is not without their hazards, however. Many pathogens enter their hosts through receptor-mediated endocytosis or phagocytosis, two intracellular trafficking pathways that terminate in a highly degradative organelle, the phagolysosome. This usually deadly compartment is maintained at a low pH and contains degradative enzymes and reactive oxygen species, resulting in an environment to which few bacterial species are adapted. Some intracellular pathogens, such as Shigella, Listeria, Francisella, and Rickettsia, escape the phagosome to replicate within the cytosol of the host cell. Bacteria that remain within a vacuole either alter the trafficking of their initial phagosomal compartment or adapt to survive within the harsh environment it will soon become. In this chapter, we focus on the mechanisms by which different vacuolar pathogens either evade lysosomal fusion, as in the case of Mycobacterium and Chlamydia, or allow interaction with lysosomes to varying degrees, such as Brucella and Coxiella, and their specific adaptations to inhabit a replicative niche.
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页数:19
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