McMaster University, Department of Biology, Life Sciences Building, Rm. 433, 1280 Main Street West, Hamilton, Ontario L8S 4K1, Canada.
Infect Immun. 2010 Mar;78(3):887-97. doi: 10.1128/IAI.00882-09. Epub 2009 Nov 30.
Understanding mechanisms of bacterial pathogenesis is critical for infectious disease control and treatment. Infection is a sophisticated process that requires the participation of global regulators to coordinate expression of not only genes coding for virulence factors but also those involved in other physiological processes, such as stress response and metabolic flux, to adapt to host environments. RpoS is a key response regulator to stress conditions in Escherichia coli and many other proteobacteria. In contrast to its conserved well-understood role in stress response, effects of RpoS on pathogenesis are highly variable and dependent on species. RpoS contributes to virulence through either enhancing survival against host defense systems or directly regulating expression of virulence factors in some pathogens, while RpoS is dispensable, or even inhibitory, to virulence in others. In this review, we focus on the distinct and niche-dependent role of RpoS in virulence by surveying recent findings in many pathogens.
了解细菌发病机制对于传染病的控制和治疗至关重要。感染是一个复杂的过程,需要全球调控器的参与,以协调不仅编码毒力因子的基因,而且还协调那些参与其他生理过程(如应激反应和代谢通量)的基因的表达,以适应宿主环境。RpoS 是大肠杆菌和许多其他变形菌中应激条件的关键反应调节剂。与应激反应中保守且理解透彻的作用相比,RpoS 对发病机制的影响差异很大,并且取决于物种。RpoS 通过增强对宿主防御系统的存活能力或直接调节某些病原体中毒力因子的表达来促进毒力,而在其他病原体中,RpoS 对毒力可有可无,甚至具有抑制作用。在这篇综述中,我们通过调查许多病原体的最新发现,重点关注 RpoS 在毒力方面的独特且依赖于小生境的作用。