Mechanosensing regulates virulence in Escherichia coli O157:H7.
Mechanosensing regulates virulence in Escherichia coli O157:H7.
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DOI：
10.1080/19490976.2015.1121365
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发表时间：
2016
期刊：
影响因子：
12.2
通讯作者：
Krachler AM
中科院分区：
文献类型：
--
作者：
Islam MS;Krachler AM
肠出血性大肠杆菌O 157：H7是一种通过粪-口途径传播的食源性病原体，可引起人类宿主出血性腹泻和溶血性尿毒综合征（HUS）。尽管一系列定植因子、滋贺毒素和III型分泌系统（T3 SS）都有助于疾病的发展，但肠上皮细胞消失（LEE）编码的T3 SS的位点负责肠道中病变的形成。虽然在宿主环境中的各种化学线索是已知的上调LEE的表达，我们最近证明，在附着位点的物理力的变化所需的本地化，充分诱导的系统，从而在肠道中的毒力的空间调节。在这里，我们讨论了我们的研究结果，在最近的其他研究中描述的机械感应的主机和力依赖性诱导的毒力机制。我们讨论了机械感应和机械转导的潜在机制，以及细菌物种之间的保护水平。
Enterohemorrhagic Escherichia coli O157:H7 is a food-borne pathogen transmitted via the fecal-oral route, and can cause bloody diarrhea and hemolytic uremic syndrome (HUS) in the human host. Although a range of colonization factors, Shiga toxins and a type III secretion system (T3SS) all contribute to disease development, the locus of enterocyte effacement (LEE) encoded T3SS is responsible for the formation of lesions in the intestinal tract. While a variety of chemical cues in the host environment are known to up-regulate LEE expression, we recently demonstrated that changes in physical forces at the site of attachment are required for localized, full induction of the system and thus spatial regulation of virulence in the intestinal tract. Here, we discuss our findings in the light of other recent studies describing mechanosensing of the host and force-dependent induction of virulence mechanisms. We discuss potential mechanisms of mechanosensing and mechanotransduction, and the level of conservation across bacterial species.