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首页> 外文期刊>Infection and immunity >The Secreted Effector Protein EspZ Is Essential for Virulence of Rabbit Enteropathogenic Escherichia coli
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The Secreted Effector Protein EspZ Is Essential for Virulence of Rabbit Enteropathogenic Escherichia coli

机译：分泌的效应蛋白EspZ对兔肠致病性大肠杆菌的毒性至关重要。

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Attaching and effacing (A/E) pathogens adhere intimately to intestinal enterocytes and efface brush border microvilli. A key virulence strategy of A/E pathogens is the type III secretion system (T3SS)-mediated delivery of effector proteins into host cells. The secreted protein EspZ is postulated to promote enterocyte survival by regulating the T3SS and/or by modulating epithelial signaling pathways. To explore the role of EspZ in A/E pathogen virulence, we generated an isogenic espZ deletion strain (ΔespZ) and corresponding cis-complemented derivatives of rabbit enteropathogenic Escherichia coli and compared their abilities to regulate the T3SS and influence host cell survival in vitro. For virulence studies, rabbits infected with these strains were monitored for bacterial colonization, clinical signs, and intestinal tissue alterations. Consistent with data from previous reports, espZ-transfected epithelial cells were refractory to infection-dependent effector translocation. Also, the ΔespZ strain induced greater host cell death than did the parent and complemented strains. In rabbit infections, fecal ΔespZ strain levels were 10-fold lower than those of the parent strain at 1 day postinfection, while the complemented strain was recovered at intermediate levels. In contrast to the parent and complemented mutants, ΔespZ mutant fecal carriage progressively decreased on subsequent days. ΔespZ mutant-infected animals gained weight steadily over the infection period, failed to show characteristic disease symptoms, and displayed minimal infection-induced histological alterations. Terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) staining of intestinal sections revealed increased epithelial cell apoptosis on day 1 after infection with the ΔespZ strain compared to animals infected with the parent or complemented strains. Thus, EspZ-dependent host cell cytoprotection likely prevents epithelial cell death and sloughing and thereby promotes bacterial colonization.
机译：附着和消灭（A / E）病原体与肠肠上皮细胞和消融刷缘微绒毛紧密粘附。 A / E病原体的关键毒力策略是III型分泌系统（T3SS）介导的效应蛋白向宿主细胞的传递。推测分泌的蛋白EspZ通过调节T3SS和/或通过调节上皮信号通路来促进肠细胞的存活。为了探索EspZ在A / E病原体毒力中的作用，我们生成了一个同基因的 espZ 缺失菌株（Δ espZ ）和相应的顺式互补比较了兔肠道致病性大肠杆菌的衍生物，并比较了它们在体外调节T3SS和影响宿主细胞存活的能力。对于毒力研究，监测感染了这些毒株的兔子的细菌定植，临床体征和肠道组织改变。与以前报道的数据一致， espZ 转染的上皮细胞难于感染依赖的效应子易位。同样，Δ espZ 菌株比亲本和互补菌株诱导更大的宿主细胞死亡。在兔感染中，粪便Δ espZ 菌株的水平在感染后1天比亲本菌株低10倍，而互补菌株在中等水平下得以恢复。与亲本和互补突变体相反，Δ espZ 突变体粪便运输在随后的几天中逐渐减少。感染Δ espZ 突变动物的体重在感染期间稳定增加，没有表现出典型的疾病症状，并且表现出最小的感染引起的组织学改变。末端脱氧核苷酸转移酶介导的肠道切片的dUTP-生物素缺口末端标记（TUNEL）染色显示，与用亲本或互补菌株感染的动物相比，用Δ espZ 菌株感染后第1天上皮细胞凋亡增加。因此，EspZ依赖性宿主细胞的细胞保护作用可能会阻止上皮细胞死亡和脱落，从而促进细菌定植。

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