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首页> 外文期刊>Infection and immunity >Regulation of Expression of Uropathogenic Escherichia coli Nonfimbrial Adhesin TosA by PapB Homolog TosR in Conjunction with H-NS and Lrp
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Regulation of Expression of Uropathogenic Escherichia coli Nonfimbrial Adhesin TosA by PapB Homolog TosR in Conjunction with H-NS and Lrp

机译：PapB同源TosR与H-NS和Lrp联合调控的致病性大肠杆菌非纤维粘附素TosA的表达

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Urinary tract infections (UTIs) are a major burden to human health. The overwhelming majority of UTIs are caused by uropathogenic Escherichia coli (UPEC) strains. Unlike some pathogens, UPEC strains do not have a fixed core set of virulence and fitness factors but do have a variety of adhesins and regulatory pathways. One such UPEC adhesin is the nonfimbrial adhesin TosA, which mediates adherence to the epithelium of the upper urinary tract. The tos operon is AT rich, resides on pathogenicity island aspV, and is not expressed under laboratory conditions. Because of this, we hypothesized that tosA expression is silenced by H-NS. Lrp, based on its prominent function in the regulation of other adhesins, is also hypothesized to contribute to tos operon regulation. Using a variety of in vitro techniques, we mapped both the tos operon promoter and TosR binding sites. We have now identified TosR as a dual regulator of the tos operon, which could control the tos operon in association with H-NS and Lrp. H-NS is a negative regulator of the tos operon, and Lrp positively regulates the tos operon. Exogenous leucine also inhibits Lrp-mediated tos operon positive regulation. In addition, TosR binds to the pap operon, which encodes another important UPEC adhesin, P fimbria. Induction of TosR synthesis reduces production of P fimbria. These studies advance our knowledge of regulation of adhesin expression associated with uropathogen colonization of a host.
机译：尿路感染（UTI）是人类健康的主要负担。绝大多数的UTI是由尿路致病性大肠埃希菌（UPEC）引起的。与某些病原体不同，UPEC菌株没有固定的毒力和适应性因子核心集，但具有多种粘附素和调控途径。一种这样的UPEC粘附素是非纤维粘附素TosA，其介导对上尿路上皮的粘附。 tos 操纵子富含AT，位于致病岛 aspV 上，在实验室条件下不表达。因此，我们假设H-NS使 tosA 表达沉默。 Lrp基于其在其他粘附素调节中的突出功能，也被认为有助于 tos 操纵子调节。使用各种体外技术，我们绘制了 tos 操纵子启动子和TosR结合位点。现在，我们已经确定TosR是 tos 操纵子的双重调节子，它可以与H-NS和Lrp一起控制 tos 操纵子。 H-NS是 tos 操纵子的负调控因子，Lrp积极地调控 tos 操纵子。外源亮氨酸还抑制Lrp介导的 tos 操纵子的正向调节。此外，TosR与 pap 操纵子结合，操纵子编码另一个重要的UPEC粘附素P菌毛。 TosR合成的诱导减少了P菌毛的产生。这些研究提高了我们对与宿主尿路致病菌定植相关的粘附素表达的调控的认识。

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