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New Aspects of RpoE in Uropathogenic Proteus mirabilis

机译：泌尿致病性变形杆菌RpoE的新方面

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Proteus mirabilis is a common human pathogen causing recurrent or persistent urinary tract infections (UTIs). The underlying mechanisms for P. mirabilis to establish UTIs are not fully elucidated. In this study, we showed that loss of the sigma factor E (RpoE), mediating extracytoplasmic stress responses, decreased fimbria expression, survival in macrophages, cell invasion, and colonization in mice but increased the interleukin-8 (IL-8) expression of urothelial cells and swarming motility. This is the first study to demonstrate that RpoE modulated expression of MR/P fimbriae by regulating mrpI, a gene encoding a recombinase controlling the orientation of MR/P fimbria promoter. By real-time reverse transcription-PCR, we found that the IL-8 mRNA amount of urothelial cells was induced significantly by lipopolysaccharides extracted from rpoE mutant but not from the wild type. These RpoE-associated virulence factors should be coordinately expressed to enhance the fitness of P. mirabilis in the host, including the avoidance of immune attacks. Accordingly, rpoE mutant-infected mice displayed more immune cell infiltration in bladders and kidneys during early stages of infection, and the rpoE mutant had a dramatically impaired ability of colonization. Moreover, it is noteworthy that urea (the major component in urine) and polymyxin B (a cationic antimicrobial peptide) can induce expression of rpoE by the reporter assay, suggesting that RpoE might be activated in the urinary tract. Altogether, our results indicate that RpoE is important in sensing environmental cues of the urinary tract and subsequently triggering the expression of virulence factors, which are associated with the fitness of P. mirabilis, to build up a UTI.
机译：奇异变形杆菌是引起复发性或持续性尿路感染（UTI）的常见人类病原体。尚未完全阐明奇异假单胞菌建立UTI的潜在机制。在这项研究中，我们发现Sigma因子E（RpoE）的丧失，介导胞浆外应激反应，菌毛表达降低，巨噬细胞存活，细胞侵袭和小鼠定植，但增加了白细胞介素8（IL-8）的表达。尿路上皮细胞和成群运动。这是第一个证明RpoE通过调节 mrpI （一种编码控制MR / P菌毛启动子方向的重组酶的基因）来调节MR / P菌毛的表达的研究。通过实时逆转录PCR，我们发现尿液中IL-8 mRNA的量是由 rpoE 突变体而非野生型提取的脂多糖显着诱导的。这些与RpoE相关的毒力因子应协调表达，以增强宿主中奇异假单胞菌的适应性，包括避免免疫攻击。因此，感染 rpoE 的小鼠在感染的早期阶段表现出更多的膀胱和肾脏免疫细胞浸润，并且 rpoE 突变体的定殖能力大大降低。此外，值得注意的是，尿液（尿液中的主要成分）和多粘菌素B（阳离子抗菌肽）可以通过报告基因检测法诱导 rpoE 的表达，表明RpoE可能在尿道中被激活。总而言之，我们的结果表明RpoE在感知尿路的环境线索并随后触发与奇异假单胞菌的适应性相关的毒力因子表达方面很重要，以建立一个UTI。

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