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沙门氏菌进入宿主细胞的机制。

Mechanisms of Salmonella entry into host cells.

作者信息

Ly Kim Thien, Casanova James E

机构信息

Department of Microbiology, University of Virginia Health System, Charlottesville, VA 22908-0732, USA.

出版信息

Cell Microbiol. 2007 Sep;9(9):2103-11. doi: 10.1111/j.1462-5822.2007.00992.x. Epub 2007 Jun 25.

Abstract

Salmonella enterica is an enteric bacterial pathogen that causes a variety of food and water-borne diseases ranging from gastroenteritis to typhoid fever. Ingested bacteria colonize the intestinal epithelium by triggering their own phagocytosis, using a sophisticated array of effector proteins that are injected into the host cell cytoplasm through a type III secretion apparatus. The synergistic action of these secreted effectors leads to a dramatic reorganization of the host actin cytoskeleton, resulting in vigorous membrane protrusion and the engulfment of attached bacteria. Analysis of these effector proteins and identification of their cellular targets has provided insight into the molecular mechanisms by which bacteria can subvert the host signalling and cytoskeletal machinery for their own purposes. This review is intended to summarize our current understanding of the tools used by Salmonella to enter host cells, with a focus on effectors that modulate the actin cytoskeleton.

摘要

肠炎沙门氏菌是一种肠道细菌病原体,可引发多种食源性和水源性疾病,范围从肠胃炎到伤寒热。摄入的细菌通过引发自身的吞噬作用来定殖于肠道上皮,利用一系列复杂的效应蛋白,这些蛋白通过III型分泌装置注入宿主细胞质中。这些分泌的效应蛋白的协同作用导致宿主肌动蛋白细胞骨架发生显著重组,从而导致有力的膜突出和附着细菌的吞噬。对这些效应蛋白的分析及其细胞靶点的鉴定,为细菌如何为自身目的颠覆宿主信号和细胞骨架机制的分子机制提供了见解。本综述旨在总结我们目前对沙门氏菌用于进入宿主细胞的工具的理解,重点是调节肌动蛋白细胞骨架的效应蛋白。

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