Furniss R Christopher D, Clements Abigail
MRC Centre for Molecular Bacteriology and Infection, Department of Life Sciences, Imperial College London, London, United Kingdom.
MRC Centre for Molecular Bacteriology and Infection, Department of Life Sciences, Imperial College London, London, United Kingdom
J Bacteriol. 2017 Dec 20;200(2). doi: 10.1128/JB.00336-17. Print 2018 Jan 15.
Attaching and effacing (AE) pathogens colonize the gut mucosa using a type three secretion system (T3SS) and a suite of effector proteins. The locus of enterocyte effacement (LEE) is the defining genetic feature of the AE pathogens, encoding the T3SS and the core effector proteins necessary for pathogenesis. Extensive research has revealed a complex regulatory network that senses and responds to a myriad of host- and microbiota-derived signals in the infected gut to control transcription of the LEE. These signals include microbiota-liberated sugars and metabolites in the gut lumen, molecular oxygen at the gut epithelium, and host hormones. Recent research has revealed that AE pathogens also recognize physical signals, such as attachment to the epithelium, and that the act of effector translocation remodels gene expression in infecting bacteria. In this review, we summarize our knowledge to date and present an integrated view of how chemical, geographical, and physical cues regulate the virulence program of AE pathogens during infection.
黏附和损伤(AE)病原体利用三型分泌系统(T3SS)和一系列效应蛋白定殖于肠道黏膜。肠上皮细胞损伤位点(LEE)是AE病原体的决定性遗传特征,编码T3SS和发病机制所需的核心效应蛋白。广泛的研究揭示了一个复杂的调控网络,该网络能感知并响应感染肠道中无数宿主和微生物群衍生的信号,以控制LEE的转录。这些信号包括肠道腔内微生物群释放的糖类和代谢产物、肠道上皮的分子氧以及宿主激素。最近的研究表明,AE病原体还能识别物理信号,如附着于上皮细胞,并且效应蛋白易位的行为会重塑感染细菌中的基因表达。在这篇综述中,我们总结了迄今为止的知识,并呈现了一个关于化学、地理和物理线索如何在感染过程中调节AE病原体毒力程序的综合观点。