Mycobacterium tuberculosis and the intimate discourse of a chronic infection.
Mycobacterium tuberculosis and the intimate discourse of a chronic infection.
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DOI：
10.1111/j.1600-065x.2010.00984.x
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发表时间：
2011-03
影响因子：
8.7
通讯作者：
Russell DG
中科院分区：
文献类型：
--
作者：
Russell DG
结核分枝杆菌是一种非常成功的病原体，其表现出在细胞和组织水平上调节其宿主的能力。在细胞水平，细菌进入其宿主巨噬细胞并阻止吞噬体成熟，从而避免与该吞噬细胞相关的许多杀微生物反应。尽管如此，细胞内环境对病原体提出了某些要求，作为回应，病原体感知环境变化并上调特定的代谢程序，以获得营养物质，最大限度地减少压力的后果，并维持感染。尽管其细胞内的生态位，结核分枝杆菌表现出显着的能力，通过释放有效的，生物活性的细胞壁成分，调节周围的组织感染的细胞。这些细胞壁脂质通过胞吐过程从宿主细胞释放，并诱导邻近吞噬细胞的生理变化，从而驱动肉芽肿的形成。这种组织反应导致干酪样碎片的产生和积累以及人结核肉芽肿的进展。肺结核生命周期的完成需要破坏宿主，将感染性细菌释放到气道中以传播感染。这种损害反映了病原体破坏宿主的先天和后天免疫反应以达到其自身邪恶目的的能力。
Mycobacterium tuberculosis is an extremely successful pathogen that demonstrates the capacity to modulate its host both at the cellular and tissue levels. At the cellular level, the bacterium enters its host macrophage and arrests phagosome maturation, thus avoiding many of the microbicidal responses associated with this phagocyte. Nonetheless, the intracellular environment places certain demands on the pathogen, which, in response, senses the environmental shifts and upregulates specific metabolic programs to allow access to nutrients, minimize the consequences of stress, and sustain infection. Despite its intracellular niche, Mycobacterium tuberculosis demonstrates a marked capacity to modulate the tissues surrounding infected cells through the release of potent, bioactive cell wall constituents. These cell wall lipids are released from the host cell by an exocytic process and induce physiological changes in neighboring phagocytes, which drives formation of a granuloma. This tissue response leads to the generation and accumulation of caseous debris and the progression of the human tuberculosis granuloma. Completion of the life cycle of tuberculosis requires damaging the host to release infectious bacteria into the airways to spread the infection. This damage reflects the pathogen’s ability to subvert the host’s innate and acquired immune responses to its own nefarious ends.