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耶尔森菌素对大肠杆菌血清型 69(“克隆群 A”)膀胱炎分离株在尿路感染和脓毒症小鼠模型中毒力的贡献。

Contribution of yersiniabactin to the virulence of an Escherichia coli sequence type 69 ("clonal group A") cystitis isolate in murine models of urinary tract infection and sepsis.

机构信息

Veterans Affairs Medical Center, 1 Veterans Drive, Minneapolis, MN, USA; University of Minnesota, 420 Delaware St. SE, MMC 250, Minneapolis, MN 55455, USA.

Department of Urology, Ludwig-Maximilians-University of Munich, Marchioninistrasse 15, 81377 Munich, Germany
.

出版信息

Microb Pathog. 2018 Jul;120:128-131. doi: 10.1016/j.micpath.2018.04.048. Epub 2018 Apr 24.

DOI:10.1016/j.micpath.2018.04.048
PMID:29702209
Abstract

Escherichia coli sequence type 69 (ST69; "clonal group A") is an important extraintestinal pathogen. To clarify the yersiniabactin siderophore system's role in ST69's extraintestinal virulence we compared a wild-type ST69 cystitis isolate, isogenic irp2 (yersiniabactin) mutants, and irp2-complemented mutants in murine models of sepsis and urinary tract infection (UTI). irp2 mutants were attenuated mildly in the UTI model and profoundly in the sepsis model. In both models, complementation with a functional copy of irp2 restored full parental virulence. These findings suggest that in ST69 the yersiniabactin system has a minor role in urovirulence and a major role in sepsis causation.

摘要

大肠杆菌序列类型 69(ST69;“克隆群 A”)是一种重要的肠外病原体。为了阐明耶尔森菌生物素铁载体系统在 ST69 肠外毒力中的作用,我们比较了野生型 ST69 膀胱炎分离株、同源 irp2(耶尔森菌生物素)突变体和 irp2 互补突变体在败血症和尿路感染(UTI)的小鼠模型中的作用。irp2 突变体在 UTI 模型中轻度减弱,在败血症模型中显著减弱。在这两种模型中,用功能完整的 irp2 基因进行互补恢复了亲本的全部毒力。这些发现表明,在 ST69 中,耶尔森菌生物素铁载体系统在尿路毒力中作用较小,而在败血症发病机制中作用较大。

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