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首页> 外文期刊>Infection and immunity >Molecular Characterization of UpaB and UpaC, Two New Autotransporter Proteins of Uropathogenic Escherichia coli CFT073
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Molecular Characterization of UpaB and UpaC, Two New Autotransporter Proteins of Uropathogenic Escherichia coli CFT073

机译：尿致病性大肠杆菌CFT073的两种新的自转运蛋白UpaB和UpaC的分子表征

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Uropathogenic Escherichia coli (UPEC) is the primary cause of urinary tract infection (UTI) in the developed world. The major factors associated with virulence of UPEC are fimbrial adhesins, which mediate specific attachment to host receptors and trigger innate host responses. Another group of adhesins is represented by the autotransporter (AT) subgroup of proteins. The genome-sequenced prototype UPEC strain CFT073 contains 11 putative AT-encoding genes. In this study, we have performed a detailed molecular characterization of two closely related AT adhesins from CFT073: UpaB (c0426) and UpaC (c0478). PCR screening revealed that the upaB and upaC AT-encoding genes are common in E. coli. The upaB and upaC genes were cloned and characterized in a recombinant E. coli K-12 strain background. This revealed that they encode proteins located at the cell surface but possess different functional properties: UpaB mediates adherence to several ECM proteins, while UpaC expression is associated with increased biofilm formation. In CFT073, upaB is expressed while upaC is transcriptionally repressed by the global regulator H-NS. In competitive colonization experiments employing the mouse UTI model, CFT073 significantly outcompeted its upaB (but not upaC) isogenic mutant strain in the bladder. This attenuated phenotype was also observed in single-challenge experiments, where deletion of the upaB gene in CFT073 significantly reduced early colonization of the bladder.
机译：致病性大肠杆菌（UPEC）是发达国家的尿路感染（UTI）的主要原因。与UPEC毒性相关的主要因素是纤维粘附素，它介导宿主受体的特异性附着并触发先天宿主反应。另一组粘附素由蛋白质的自转运子（AT）亚组代表。基因组测序的原型UPEC菌株CFT073包含11个假定的AT编码基因。在这项研究中，我们对CFT073中两个紧密相关的AT粘附素进行了详细的分子表征：UpaB（c0426）和UpaC（c0478）。 PCR筛选显示upaB和upaC AT编码基因在大肠杆菌中很常见。在重组大肠杆菌K-12菌株背景中克隆了upaB和upaC基因并对其进行了表征。这表明它们编码位于细胞表面的蛋白质，但具有不同的功能特性：UpaB介导对几种ECM蛋白质的粘附，而UpaC的表达与生物膜形成增加有关。在CFT073中，表达了upaB，而全局调节剂H-NS转录了对upaC的抑制。在采用小鼠UTI模型的竞争性定植实验中，CFT073在膀胱中明显优于其upaB（但不是upaC）同基因突变株。在单攻击实验中也观察到了这种减弱的表型，其中CFT073中upaB基因的缺失显着降低了膀胱的早期定植。

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