Department of Microbiology and Physiological Systems, The University of Massachusetts Medical School, Worcester, MA 01655, USA.
Cell Mol Life Sci. 2011 Nov;68(22):3687-97. doi: 10.1007/s00018-011-0841-0. Epub 2011 Oct 9.
Acute gastroenteritis caused by Salmonella enterica serovar typhimurium is a significant public health problem. This pathogen has very sophisticated molecular machinery encoded by the two pathogenicity islands, namely Salmonella Pathogenicity Island 1 and 2 (SPI-1 and SPI-2). Remarkably, both SPI-1 and SPI-2 are very tightly regulated in terms of timing of expression and spatial localization of the encoded effectors during the infection process within the host cell. This regulation is governed at several levels, including transcription and translation, and by post-translational modifications. In the context of a finely tuned regulatory system, we will highlight how these effector proteins co-opt host signaling pathways that control the ability of the organism to infect and survive within the host, as well as elicit host pro-inflammatory responses.
鼠伤寒沙门氏菌引起的急性肠胃炎是一个重大的公共卫生问题。这种病原体具有非常复杂的分子机制,由两个致病性岛(SPI-1 和 SPI-2)编码。值得注意的是,SPI-1 和 SPI-2 在感染宿主细胞的过程中,无论是在表达时间还是在编码效应子的空间定位方面,都受到非常严格的调控。这种调控在多个水平上进行,包括转录和翻译,以及翻译后修饰。在精细调控系统的背景下,我们将重点介绍这些效应蛋白如何共同利用宿主信号通路来控制生物体感染和在宿主内存活的能力,并引发宿主的促炎反应。