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鼬螺杆菌和幽门螺杆菌在体外可与共同的脂质受体结合。

Helicobacter mustelae and Helicobacter pylori bind to common lipid receptors in vitro.

作者信息

Gold B D, Huesca M, Sherman P M, Lingwood C A

机构信息

Division of Gastroenterology, Research Institute, Hospital for Sick Children, Toronto, Ontario, Canada.

出版信息

Infect Immun. 1993 Jun;61(6):2632-8. doi: 10.1128/iai.61.6.2632-2638.1993.

DOI:10.1128/iai.61.6.2632-2638.1993
PMID:8500901
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC280894/
Abstract

Helicobacter pylori is a recently recognized human pathogen causing chronic-active gastritis in association with duodenal ulcers and gastric cancer. Helicobacter mustelae is a closely related bacterium with similar biochemical and morphologic characteristics. H. mustelae infection of antral and fundic mucosa in adult ferrets causes chronic gastritis. An essential virulence property of both Helicobacter species is bacterial adhesion to mucosal surfaces. The aim of this study was to determine whether H. mustelae binds to the same lipids shown previously to be receptors for H. pylori adhesion in vitro. By using thin-layer chromatography overlay and a receptor-based enzyme-linked immunosorbent assay, H. mustelae was found to bind the same receptor lipids as H. pylori, namely, phosphatidylethanolamine and gangliotetraosylceramide. In addition, both H. pylori and H. mustelae bound to a deacylplasmalogen phosphatidylethanolamine. In contrast to H. pylori, H. mustelae binding to receptors was unaffected by motility or viability. Murine monoclonal and bovine polyclonal antibodies against exoenzyme S, and exoenzyme S itself (from Pseudomonas aeruginosa), inhibited binding of H. mustelae to phosphatidylethanolamine and gangliotetraosylceramide. These findings show that H. mustelae binds in vitro to the same lipid receptors as H. pylori and suggest that the adhesion of H. mustelae to such species is mediated by preformed, surface-exposed adhesins which include an exoenzyme S-like protein.

摘要

幽门螺杆菌是一种最近才被认识的人类病原体,可导致与十二指肠溃疡和胃癌相关的慢性活动性胃炎。鼬螺杆菌是一种密切相关的细菌,具有相似的生化和形态学特征。成年雪貂的胃窦和胃底黏膜感染鼬螺杆菌会导致慢性胃炎。这两种幽门螺杆菌的一个基本毒力特性是细菌黏附于黏膜表面。本研究的目的是确定鼬螺杆菌是否与先前在体外被证明是幽门螺杆菌黏附受体的相同脂质结合。通过使用薄层层析覆盖法和基于受体的酶联免疫吸附测定,发现鼬螺杆菌与幽门螺杆菌结合相同的受体脂质,即磷脂酰乙醇胺和神经节四糖神经酰胺。此外,幽门螺杆菌和鼬螺杆菌都与脱酰基缩醛磷脂酰乙醇胺结合。与幽门螺杆菌不同,鼬螺杆菌与受体的结合不受运动性或活力的影响。针对外毒素S的鼠单克隆抗体和牛多克隆抗体,以及外毒素S本身(来自铜绿假单胞菌),均可抑制鼬螺杆菌与磷脂酰乙醇胺和神经节四糖神经酰胺的结合。这些发现表明,鼬螺杆菌在体外与幽门螺杆菌结合相同的脂质受体,并表明鼬螺杆菌对这些物质的黏附是由预先形成的、表面暴露的黏附素介导的,其中包括一种外毒素S样蛋白。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d07a/280894/1fce5e937355/iai00018-0377-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d07a/280894/fe1bddb6f2f9/iai00018-0376-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d07a/280894/cf010d7f7dd2/iai00018-0377-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d07a/280894/1fce5e937355/iai00018-0377-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d07a/280894/fe1bddb6f2f9/iai00018-0376-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d07a/280894/cf010d7f7dd2/iai00018-0377-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d07a/280894/1fce5e937355/iai00018-0377-b.jpg

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