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宿主对志贺氏菌分泌的毒力因子的反应。

Host responses to secreted Shigella virulence factors.

作者信息

Hilbi H

机构信息

Skirball Institute, Department of Microbiology, New York University Medical Center, New York, NY 10016, USA.

出版信息

Curr Opin Infect Dis. 1999 Jun;12(3):221-8. doi: 10.1097/00001432-199906000-00011.

Abstract

Shigella and related enteropathogens deliver effector molecules into the cytoplasm of epithelial cells and macrophages via a type III secretion system. Epithelial cells respond to contact with Shigella by rearranging the cytoskeleton, which leads to uptake of the bacterium. Apart from several cytoskeletal proteins, this process involves the recruitment and activation of kinases, and the small GTPase rho. Macrophages infected with Shigella undergo apoptosis and release mature IL-1beta, a pro-inflammatory cytokine. This apoptotic pathway requires caspase-1 (IL-1beta-converting enzyme). Pro-inflammatory macrophage apoptosis triggers acute shigellosis and might be relevant in other infectious diseases.

摘要

志贺氏菌及相关肠道病原体通过III型分泌系统将效应分子输送到上皮细胞和巨噬细胞的细胞质中。上皮细胞通过重新排列细胞骨架对与志贺氏菌的接触做出反应,这会导致细菌被摄取。除了几种细胞骨架蛋白外,这个过程还涉及激酶和小GTP酶rho的募集和激活。感染志贺氏菌的巨噬细胞会发生凋亡并释放成熟的促炎细胞因子IL-1β。这种凋亡途径需要caspase-1(IL-1β转化酶)。促炎性巨噬细胞凋亡引发急性志贺氏菌病,可能与其他传染病有关。

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