Caron Emmanuelle, Crepin Valerie F, Simpson Nandi, Knutton Stuart, Garmendia Junkal, Frankel Gad
Centre for Molecular Microbiology and Infection, Division of Cell and Molecular Biology, Imperial College London, London SW7 2AZ, UK.
Curr Opin Microbiol. 2006 Feb;9(1):40-5. doi: 10.1016/j.mib.2005.12.008. Epub 2006 Jan 6.
During the course of infection, enteropathogenic and enterohaemorrhagic Escherichia coli (EPEC and EHEC, respectively) subvert the host cell signalling machinery and hijack the actin cytoskeleton to tighten their interaction with the gut epithelium, while avoiding phagocytosis by professional phagocytes. Much progress has been made recently in our understanding of how EPEC and EHEC regulate the pathways leading to local activation of two regulators of actin cytoskeleton dynamics, the Wiskott-Aldrich syndrome protein (N-WASP) and the Arp2/3 complex. A recent highlight is the unravelling of functions for effector proteins (particularly Tir, TccP, Map and EspG/EspG2) that are injected into the host cell by a type III secretion system.
在感染过程中，肠道致病性大肠杆菌和肠出血性大肠杆菌（分别为EPEC和EHEC）破坏宿主细胞信号传导机制并劫持肌动蛋白细胞骨架，以加强它们与肠道上皮的相互作用，同时避免被专职吞噬细胞吞噬。最近，我们在了解EPEC和EHEC如何调节导致肌动蛋白细胞骨架动力学的两个调节因子（威斯科特-奥尔德里奇综合征蛋白（N-WASP）和Arp2/3复合体）局部激活的途径方面取得了很大进展。最近的一个亮点是揭示了通过III型分泌系统注入宿主细胞的效应蛋白（特别是Tir、TccP、Map和EspG/EspG2）的功能。
