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志贺氏菌感染肠道上皮细胞和规避宿主先天防御系统。

Shigella infection of intestinal epithelium and circumvention of the host innate defense system.

机构信息

Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, Japan.

出版信息

Curr Top Microbiol Immunol. 2009;337:231-55. doi: 10.1007/978-3-642-01846-6_8.

Abstract

Shigella, Gram-negative bacteria closely related to Escherichia coli, are highly adapted human pathogens that cause bacillary dysentery. Although Shigella have neither adherence factors nor flagella required for attaching or accessing the intestinal epithelium, Shigella are capable of colonizing the intestinal epithelium by exploiting epithelial-cell functions and circumventing the host innate immune response. During Shigella infection, they deliver many numbers of effectors through the type III secretion system into the surrounding space and directly into the host-cell cytoplasm. The effectors play pivotal roles from the onset of bacterial infection through to the establishment of the colonization of the intestinal epithelium, such as bacterial invasion, intracellular survival, subversion of the host immune defense response, and maintenance of the infectious foothold. These examples suggest that Shigella have evolved highly sophisticated infectious and intracellular strategies to establish replicative niches in the intestinal epithelium.

摘要

志贺氏菌是与大肠杆菌关系密切的革兰氏阴性细菌,是高度适应人体的病原体,可引起细菌性痢疾。尽管志贺氏菌既没有附着因子也没有鞭毛来附着或进入肠上皮,但志贺氏菌能够通过利用肠上皮细胞的功能并规避宿主先天免疫反应来定殖肠上皮。在志贺氏菌感染过程中,它们通过 III 型分泌系统将大量效应子输送到周围空间,并直接输送到宿主细胞质中。这些效应子在细菌感染的起始到肠上皮定植的建立过程中发挥着关键作用,如细菌入侵、细胞内生存、颠覆宿主免疫防御反应以及维持感染立足点。这些例子表明,志贺氏菌已经进化出高度复杂的感染和细胞内策略,以在肠上皮中建立复制龛。

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