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The Gal(alpha 1-4)Gal-specific tip adhesin of Escherichia coli P-fimbriae is needed for pyelonephritis to occur in the normal urinary tract.

机译:大肠杆菌P-菌毛的Gal(alpha 1-4)Gal特异性末端粘附素是肾盂肾炎在正常泌尿道发生的必要条件。

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摘要

Nonobstructive acute pyelonephritis in humans is most often caused by P-fimbriated Escherichia coli. P-fimbriae are heteropolymeric fibers carrying a Gal(alpha 1-4)Gal-specific PapG adhesin at its distal end. The pyelonephritic strain DS17 expresses P-fimbriae from a single gene cluster. A mutant strain, DS17-8, which expresses P-fimbriae tacking the PapG adhesin, was constructed by allelic replacement introducing a 1-bp deletion early in the papG gene. In cynomolgus monkeys, DS17 and DS17-8 were equally able to cause bladder infection, whereas only the wild-type strain DS17 could cause pyelonephritis as monitored by bacteriological, functional, and histopathological criteria. Since DS17, but not DS17-8, adheres to renal tissue, these data underscore the critical role of microbial adherence to host tissues in infectious disease and strongly suggest that the PapG tip adhesin of P-fimbriae is essential in the pathogenesis of human kidney infection.
机译:人的非阻塞性急性肾盂肾炎最常见是由P纤维化大肠杆菌引起的。 P-菌毛是在其远端带有Gal(alpha 1-4)Gal特异性PapG粘附素的杂聚合纤维。肾盂肾炎菌株DS17从单个基因簇表达P-菌毛。通过等位基因置换,在papG基因的早期引入1-bp缺失,构建了表达P-菌毛附着PapG粘附素的突变株DS17-8。在食蟹猴中,DS17和DS17-8同样能够引起膀胱感染,而通过细菌学,功能和组织病理学标准监测,只有野生型DS17可以引起肾盂肾炎。由于DS17而不是DS17-8附着在肾脏组织上,因此这些数据强调了微生物附着在宿主组织中在传染性疾病中的关键作用,并强烈暗示P-菌毛的PapG尖端粘附素在人类肾脏感染的发病机理中至关重要。

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