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Suppression of Bladder Epithelial Cytokine Responses by Uropathogenic Escherichia coli

机译：尿毒症性大肠杆菌抑制膀胱上皮细胞因子的反应

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Urinary tract infections are most commonly caused by uropathogenic strains of Escherichia coli (UPEC), which invade superficial bladder epithelial cells via a type 1 pilus-dependent mechanism. Inside these epithelial cells, UPEC organisms multiply to high numbers to form intracellular bacterial communities, allowing them to avoid immune detection. Bladder epithelial cells produce interleukin-6 (IL-6) and IL-8 in response to laboratory strains of E. coli in vitro. We investigated the ability of UPEC to alter epithelial cytokine signaling by examining the in vitro responses of bladder epithelial cell lines to the cystitis strains UTI89 and NU14. The cystitis strains induced significantly less IL-6 than did the laboratory E. coli strain MG1655 from 5637 and T24 bladder epithelial cells. The cystitis strains also suppressed epithelial cytokine responses to exogenous lipopolysaccharide (LPS) and to laboratory E. coli. We found that insertional mutations in the rfa and rfb operons and in the surA gene all abolished the ability of UTI89 to suppress cytokine induction. The rfa and rfb operons encode LPS biosynthetic genes, while surA encodes a periplasmic cis-trans prolyl isomerase important in the biogenesis of outer membrane proteins. We conclude that, in this in vitro model system, cystitis strains of UPEC have genes encoding factors that suppress proinflammatory cytokine production by bladder epithelial cells.
机译：尿路感染最常见是由大肠杆菌（UPEC）的泌尿道致病菌株引起的，该菌株通过1型菌毛依赖性机制侵袭浅表膀胱上皮细胞。在这些上皮细胞内部，UPEC生物大量繁殖形成细胞内细菌群落，从而避免了免疫检测。膀胱上皮细胞产生白细胞介素6（IL-6）和白细胞介素8，以应对 E实验室菌株。大肠杆菌。我们通过检查膀胱上皮细胞系对膀胱炎菌株UTI89和NU14的体外反应，研究了UPEC改变上皮细胞因子信号传导的能力。膀胱炎菌株诱导的IL-6明显少于实验室Eem。来自5637和T24膀胱上皮细胞的大肠杆菌MG1655菌株。膀胱炎菌株还抑制了上皮细胞因子对外源脂多糖（LPS）和实验室E的反应。大肠杆菌。我们发现 rfa 和 rfb 操纵子以及 surA 基因中的插入突变均消除了UTI89抑制细胞因子诱导的能力。 rfa 和 rfb 操纵子编码LPS生物合成基因，而 surA 编码在细胞中重要的周质顺-反脯氨酰异构酶。外膜蛋白的生物发生。我们得出的结论是，在此体外模型系统中，UPEC膀胱炎菌株具有的基因编码抑制膀胱上皮细胞促炎性细胞因子产生的因子。

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