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首页> 外文期刊>Infection and immunity >Translocated Intimin Receptors (Tir) of Shiga-Toxigenic Escherichia coli Isolates Belonging to Serogroups O26, O111, and O157 React with Sera from Patients with Hemolytic-Uremic Syndrome and Exhibit Marked Sequence Heterogeneity
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Translocated Intimin Receptors (Tir) of Shiga-Toxigenic Escherichia coli Isolates Belonging to Serogroups O26, O111, and O157 React with Sera from Patients with Hemolytic-Uremic Syndrome and Exhibit Marked Sequence Heterogeneity

机译：属于志贺毒素的大肠埃希菌大肠杆菌的易位内膜受体（Tir）属于血清型O26，O111和O157，与溶血性尿毒症综合征并表现出明显的序列异质性

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The capacity to form attaching and effacing (A/E) lesions on the surfaces of enterocytes is an important virulence trait of several enteric pathogens, including enteropathogenic Escherichia coli (EPEC) and Shiga-toxigenic E. coli (STEC). Formation of such lesions depends upon an interaction between a bacterial outer membrane protein (intimin) and a bacterially encoded receptor protein (Tir) which is exported from the bacterium and translocated into the host cell membrane. Intimin, Tir, and several other proteins necessary for generation of A/E lesions are encoded on a chromosomal pathogenicity island termed the locus for enterocyte effacement (LEE). Reports of sequence heterogeneity and antigenic variation in the region of intimin believed to be responsible for receptor binding raise the possibility that the receptor itself is also heterogeneous. We have examined this by cloning and sequencingtir genes from three different STEC strains belonging to serogroups O26, O111, and O157. The deduced amino acid sequences for the Tir homologues from these strains varied markedly, exhibiting only 65.4, 80.2, and 56.7% identity, respectively, to that recently reported for EPEC Tir. STEC Tir is also highly immunogenic in humans. Western blots of E. coli DH5α expressing the various STECtir genes cloned in pBluescript [but not E. coli DH5α(pBluescript)] reacted strongly with convalescent sera from patients with hemolytic-uremic syndrome (HUS) caused by known LEE-positive STEC. Moreover, no reaction was seen when the various clone lysates were probed with serum from a patient with HUS caused by a LEE-negative STEC or with serum from a healthy individual. Covariation of exposed epitopes on both intimin and Tir may be a means whereby STEC avoid host immune responses without compromising adhesin-receptor interaction.
机译：在肠上皮细胞表面形成附着和消融（A / E）损伤的能力是几种肠道病原体的重要毒力特征，其中包括肠道致病性大肠杆菌（EPEC）和志贺毒素 E 。大肠菌（STEC）。这种损伤的形成取决于细菌外膜蛋白（内膜素）和细菌编码的受体蛋白（Tir）之间的相互作用，该蛋白从细菌中输出并转移到宿主细胞膜中。内膜素，Tir和其他一些产生A / E损伤所必需的蛋白质被编码在染色体致病岛上，该岛被称为肠上皮细胞出现（LEE）的场所。关于内膜蛋白区域中序列异质性和抗原变异的报道被认为是受体结合的原因，这增加了受体本身也是异质性的可能性。我们已经通过克隆和测序来自三个不同STEC菌株的基因 tir 进行了检验，这些菌株分别属于O26，O111和O157血清群。从这些菌株推导的Tir同系物的氨基酸序列显着变化，与最近报道的EPEC Tir相比，分别仅表现出65.4、80.2和56.7％的同一性。 STEC Tir在人类中也具有高度免疫原性。 E的Western印迹。大肠杆菌DH5α表达克隆在pBluescript中的各种STEC tir 基因[但不是 E。 DH5α（pBluescript）]与已知的LEE阳性STEC引起的溶血性尿毒症综合征（HUS）患者的恢复期血清发生强烈反应。此外，当用LEE阴性STEC引起的HUS患者血清或健康个体的血清探查各种克隆裂解液时，未见反应。内膜蛋白和Tir上暴露表位的共变可能是STEC避免宿主免疫反应而不损害粘附素-受体相互作用的一种手段。

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