Vibrio cholerae persistence in aquatic environments and colonization of intestinal cells: involvement of a common adhesion mechanism
Author(s) -
Zampini Massimiliano,
Pruzzo Carla,
Bondre Vijay P.,
Tarsi Renato,
Cosmo Mariangela,
Bacciaglia Alessandro,
Chhabra Arvind,
Srivastava Renjana,
Srivastava Brahm S.
Publication year - 2005
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1016/j.femsle.2005.01.052
Subject(s) - vibrio cholerae , microbiology and biotechnology , mutant , chitin , cd81 , biofilm , strain (injury) , biology , colonization , adhesion , caco 2 , bacterial adhesin , bacteria , food science , chemistry , biochemistry , cell , escherichia coli , genetics , gene , hepatitis c virus , virus , organic chemistry , anatomy , chitosan
Forty‐one Tn pho A mutants of Vibrio cholerae O1 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.
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