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肠致病性大肠杆菌与人肠道器官培养物相互作用中由紧密黏附素介导的组织特异性

Intimin-mediated tissue specificity in enteropathogenic Escherichia coli interaction with human intestinal organ cultures.

作者信息

Phillips A D, Frankel G

机构信息

University Department of Paediatric Gastroenterology, Royal Free Hospital, London NW3 2QG, United Kingdom.

出版信息

J Infect Dis. 2000 Apr;181(4):1496-500. doi: 10.1086/315404. Epub 2000 Apr 13.

Abstract

The hallmark of enterohemorrhagic Escherichia coli (EHEC) and enteropathogenic E. coli (EPEC) adhesion to cultured human host cells is intimate attachment and the formation of attaching and effacing (A/E) lesions. Recently, EHEC O157:H7 was shown to induce A/E lesions on human intestinal explants. Unlike EPEC, which colonized the small intestine, EHEC adhesion was restricted to follicle-associated epithelium (FAE) of ileal Peyer's patches. This study tested the hypothesis that the bacterial adhesin intimin contributes to tissue specificity. Complementing the eae gene mutation in CVD206 (derived from EPEC strain E2348/69) with EPEC eaealpha (encoding intimin-alpha) restored the ability to colonize small intestinal mucosa like the parent strain. In contrast, complementing with EHEC eaegamma (encoding intimin-gamma) resulted in the strain adhering and inducing A/E lesion on Peyer's patches, similar to EHEC. An intimin-gamma-positive O55:H7 EPEC also targeted FAE. Thus, intimin contributes to the tissue specificity of A/E lesion-forming microbial pathogens.

摘要

肠出血性大肠杆菌(EHEC)和肠致病性大肠杆菌(EPEC)黏附于培养的人类宿主细胞的标志是紧密附着以及形成黏附与抹平(A/E)损伤。最近研究表明,EHEC O157:H7可在人肠道外植体上诱导A/E损伤。与定殖于小肠的EPEC不同,EHEC的黏附局限于回肠派尔集合淋巴结的滤泡相关上皮(FAE)。本研究检验了细菌黏附素紧密黏附素促成组织特异性这一假说。用EPEC eaeα(编码紧密黏附素α)补充CVD206(源自EPEC菌株E2348/69)中的eae基因突变,可恢复其定殖于小肠黏膜的能力,与亲本菌株相似。相比之下,用EHEC eaegamma(编码紧密黏附素γ)补充则导致该菌株在派尔集合淋巴结上黏附并诱导A/E损伤,与EHEC相似。一株紧密黏附素γ阳性的O55:H7 EPEC也靶向FAE。因此,紧密黏附素促成了形成A/E损伤的微生物病原体的组织特异性。

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