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Vibrio cholerae persistence in aquatic environments and colonization of intestinal cells: involvement of a common adhesion mechanism

机译:霍乱弧菌在水生环境中的持久性和肠道细胞的定殖:共同的粘附机制的参与

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摘要

Forty-one Tnpho A mutants of Vibrio cholerae 01 classical strain CD81 were analyzed for their ability to interact with chitin particles, Tigriopus fulvus copepods and the Intestine 407 cell line compared to the parent strain. Thirteen mutants were less adhesive than CD81; in particular, T21, T33 and T87 were less adhesive towards all substrates and insensitive to inhibition by N-acetyl glucosamine (GlcNAc). By SDS-PAGE analysis of sarkosyl-insoluble membrane proteins (siMPs) isolated from mutants and parent, it was found that a 53 kDa siMP is missing in T21, T33 and T87 mutants. It is hypothesized that this protein might have the function to mediate adherence to GlcNAc-containing substrates both in the aquatic environment and in human intestine. (c) 2005 Federation of European Microbiological Societies. Published by Elsevier B.V. All rights reserved.
机译:与亲本菌株相比,分析了霍乱弧菌01经典菌株CD81的41个Tnpho A突变体与几丁质颗粒,黄花Ti足co和肠道407细胞系相互作用的能力。 13个突变体的黏附性低于CD81。特别是,T21,T33和T87对所有底物的粘合性较小,并且对N-乙酰基氨基葡萄糖(GlcNAc)的抑制不敏感。通过对分离自突变体和亲本的沙克糖基不溶性膜蛋白(siMP)的SDS-PAGE分析,发现在T21,T33和T87突变体中缺失了53 kDa siMP。假设该蛋白可能具有在水生环境和人肠中介导对含GlcNAc底物的粘附的功能。 (c)2005年欧洲微生物学会联合会。由Elsevier B.V.发布。保留所有权利。

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