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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Filamentation by Escherichia coli subverts innate defenses during urinary tract infection
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Filamentation by Escherichia coli subverts innate defenses during urinary tract infection

机译：大肠杆菌的纤维化破坏了尿路感染期间的先天防御

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摘要

To establish disease, an infecting organism must overcome a vast array of host defenses. During cystitis, uropathogenic Escherichia coli (UPEC) subvert innate defenses by invading superficial umbrella cells and rapidly increasing in numbers to form intracelluiar bacterial communities (IBCs). In the late stages of the IBC pathway, filamentous and bacillary UPEC detach from the biofilm-like IBC, fluxing out of this safe haven to colonize the surrounding epithelium and initiate subsequent generations of IBCs, and eventually they establish a quiescent intracelluiar reservoir. Filamentous UPEC are not observed during acute infection in mice lacking functional Toll-like receptor 4 (TLR4), suggesting that the filamentous phe-notype arises in response to host innate immunity. We investigated SulA, a cell division inhibitor associated with the SOS response, to gain insight into the role of filamentous UPEC in pathogenesis. A transcriptional reporter from Psuia revealed spatial and temporal differences in expression within IBCs, and it was active in the majority of filamentous UPEC. Although UTI89 and UTI89 ΔsulA both formed first-generation IBCs equally well, UTI89 ΔsulA was sharply attenuated in formation of second-generation IBCs and establishment of the quiescent intracelluiar reservoir. The virulence of UTI89 ΔsulA was restored in TLR4-deficient mice, suggesting that filamentation facilitates the transition to additional rounds of IBC formation by subverting innate immune responses. These findings demonstrate that transient SulA-medi-ated inhibition of cell division is essential for UPEC virulence in the murine model of cystitis.
机译：为了确定疾病，感染性生物必须克服各种各样的宿主防御。在膀胱炎期间，尿路致病性大肠埃希氏菌（UPEC）通过侵入浅层伞状细胞并迅速增加其数量以形成细胞内细菌群落（IBC），从而破坏了先天防御。在IBC通路的后期，丝状和细菌性UPEC从生物膜状IBC脱离，从这个安全港逃逸出来，定居在周围的上皮中，并引发随后的IBC生成，并最终建立了一个静止的细胞内储液池。缺乏功能性Toll样受体4（TLR4）的小鼠在急性感染过程中未观察到丝状UPEC，这表明丝状phe-notype响应宿主的先天免疫而出现。我们研究了SulA，一种与SOS反应相关的细胞分裂抑制剂，以深入了解丝状UPEC在发病机理中的作用。来自Psuia的转录报告基因揭示了IBC内表达的时空差异，并且在大多数丝状UPEC中活跃。尽管UTI89和UTI89ΔsulA均能很好地形成第一代中型散货箱，但第二代中型散货箱的形成和静态细胞内储库的建立大大削弱了UTI89ΔsulA。在TLR4缺陷型小鼠中恢复了UTI89ΔsulA的毒力，这表明细丝化通过破坏先天免疫应答而促进了向其他IBC形成轮的过渡。这些发现表明，在膀胱炎小鼠模型中，SulA介导的细胞分裂的短暂抑制对于UPEC毒力至关重要。

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