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幽门螺杆菌和鼬獾螺杆菌同基因鞭毛阴性突变体对人和雪貂胃上皮细胞的黏附

Adherence of isogenic flagellum-negative mutants of Helicobacter pylori and Helicobacter mustelae to human and ferret gastric epithelial cells.

作者信息

Clyne M, Ocroinin T, Suerbaum S, Josenhans C, Drumm B

机构信息

Department of Paediatrics and The Conway Institute of Molecular and Biomedical Research, University College Dublin, Belfield, Dublin 4, Ireland.

出版信息

Infect Immun. 2000 Jul;68(7):4335-9. doi: 10.1128/IAI.68.7.4335-4339.2000.

DOI:10.1128/IAI.68.7.4335-4339.2000
PMID:10858255
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC101762/
Abstract

Isogenic flagellum-negative mutants of Helicobacter pylori and Helicobacter mustelae were screened for their ability to adhere to primary human and ferret gastric epithelial cells, respectively. We also evaluated the adherence of an H. pylori strain with a mutation in the flbA gene, a homologue of the flbF/lcrD family of genes known to be involved in the regulation of H. pylori flagellar biosynthesis. H. pylori and H. mustelae mutants deficient in production of FlaA or FlaB and mutants deficient in the production of both FlaA and FlaB showed no reduction in adherence to primary human or ferret gastric epithelial cells compared with the wild-type parental strains. However, adherence of the H. pylori flbA mutant to human gastric cells was significantly reduced compared to the adherence of the wild-type strain. These results show that flagella do not play a direct role in promoting adherence of H. pylori or H. mustelae to gastric epithelial cells. However, genes involved in the regulation of H. pylori flagellar biosynthesis may also regulate the production of an adhesin.

摘要

分别筛选了幽门螺杆菌和鼬獾幽门螺杆菌的同基因鞭毛阴性突变体,以检测它们分别黏附原代人胃上皮细胞和雪貂胃上皮细胞的能力。我们还评估了flbA基因发生突变的幽门螺杆菌菌株的黏附情况,flbA基因是flbF/lcrD基因家族的同源基因,已知该基因家族参与幽门螺杆菌鞭毛生物合成的调控。与野生型亲本菌株相比,缺乏FlaA或FlaB产生的幽门螺杆菌和鼬獾幽门螺杆菌突变体以及同时缺乏FlaA和FlaB产生的突变体,在黏附原代人或雪貂胃上皮细胞方面没有降低。然而,与野生型菌株的黏附情况相比,幽门螺杆菌flbA突变体对人胃细胞的黏附显著降低。这些结果表明,鞭毛在促进幽门螺杆菌或鼬獾幽门螺杆菌黏附胃上皮细胞方面不发挥直接作用。然而,参与幽门螺杆菌鞭毛生物合成调控的基因也可能调控黏附素的产生。

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本文引用的文献

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