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伯克霍尔德氏菌属假单胞菌的胞内生存策略。

Strategies for Intracellular Survival of Burkholderia pseudomallei.

机构信息

Department of Microbiology, Monash University Clayton, VIC, Australia.

出版信息

Front Microbiol. 2011 Aug 22;2:170. doi: 10.3389/fmicb.2011.00170. eCollection 2011.

DOI:10.3389/fmicb.2011.00170
PMID:22007185
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3159172/
Abstract

Burkholderia pseudomallei is the causative agent of melioidosis, a disease with high mortality that is prevalent in tropical regions of the world. A key component of the pathogenesis of melioidosis is the ability of B. pseudomallei to enter, survive, and replicate within mammalian host cells. For non-phagocytic cells, bacterial adhesins have been identified both on the bacterial surface and associated with Type 4 pili. Cell invasion involves components of one or more of the three Type 3 Secretion System clusters, which also mediate, at least in part, the escape of bacteria from the endosome into the cytoplasm, where bacteria move by actin-based motility. The mechanism of actin-based motility is not clearly understood, but appears to differ from characterized mechanisms in other bacterial species. A small proportion of intracellular bacteria is targeted by host cell autophagy, involving direct recruitment of LC3 to endosomes rather than through uptake by canonical autophagosomes. However, the majority of bacterial cells are able to circumvent autophagy and other intracellular defense mechanisms such as the induction of inducible nitric oxide synthase, and then replicate in the cytoplasm and spread to adjacent cells via membrane fusion, resulting in the formation of multi-nucleated giant cells. A potential role for host cell ubiquitin in the autophagic response to bacterial infection has recently been proposed.

摘要

类鼻疽伯克霍尔德菌是类鼻疽病的病原体,该病死亡率高,在世界热带地区流行。类鼻疽病发病机制的一个关键组成部分是类鼻疽伯克霍尔德菌进入、存活和在哺乳动物宿主细胞内复制的能力。对于非吞噬细胞,细菌黏附素不仅存在于细菌表面,而且与 IV 型菌毛相关。细胞入侵涉及一种或多种 III 型分泌系统簇的成分,这些成分至少部分介导细菌从内体逃逸到细胞质,在细胞质中,细菌通过肌动蛋白依赖性运动移动。肌动蛋白依赖性运动的机制尚不清楚,但似乎与其他细菌物种中已确定的机制不同。一小部分细胞内细菌被宿主细胞自噬靶向,涉及 LC3 直接募集到内体,而不是通过经典自噬体摄取。然而,大多数细菌细胞能够逃避自噬和其他细胞内防御机制,如诱导诱导型一氧化氮合酶,然后在细胞质中复制,并通过膜融合在邻近细胞中扩散,导致多核巨细胞的形成。最近提出了宿主细胞泛素在细菌感染的自噬反应中的潜在作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea0c/3159172/f03054da2234/fmicb-02-00170-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea0c/3159172/7197a3b0e0ef/fmicb-02-00170-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea0c/3159172/f03054da2234/fmicb-02-00170-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea0c/3159172/7197a3b0e0ef/fmicb-02-00170-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea0c/3159172/f03054da2234/fmicb-02-00170-g002.jpg

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