原创力文档vibrio cholerae vexh encodes a multiple drug efflux pump that contributes to the production of cholera toxin and the toxin co-regulated pilus霍乱弧菌vexh编码多个药物外排泵,导致霍乱毒素的生产和毒素重新纤毛.pdfVIP
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vibrio cholerae vexh encodes a multiple drug efflux pump that contributes to the production of cholera toxin and the toxin co-regulated pilus霍乱弧菌vexh编码多个药物外排泵,导致霍乱毒素的生产和毒素重新纤毛
Vibrio cholerae vexH Encodes a Multiple Drug Efflux
Pump That Contributes to the Production of Cholera
Toxin and the Toxin Co-Regulated Pilus
Dawn L. Taylor, Xiaowen R. Bina, James E. Bina*
University of Pittsburgh School of Medicine, Department of Microbiology and Molecular Genetics, Pittsburgh, Pennsylvania, United States of America
Abstract
The resistance-nodulation-division (RND) efflux systems are ubiquitous transporters that function in antimicrobial resistance.
Recent studies showed that RND systems were required for virulence factor production in Vibrio cholerae. The V. cholerae
genome encodes six RND efflux systems. Three of the RND systems (VexB, VexD, and VexK) were previously shown to be
redundant for in vitro resistance to bile acids and detergents. A mutant lacking the VexB, VexD, and VexK RND pumps
produced wild-type levels of cholera toxin (CT) and the toxin co-regulated pilus (TCP) and was moderately attenuated for
intestinal colonization. In contrast, a RND negative mutant produced significantly reduced amounts of CT and TCP and
displayed a severe colonization defect. This suggested that one or more of the three uncharacterized RND efflux systems
(i.e. VexF, VexH, and VexM) were required for pathogenesis. In this study, a genetic approach was used to generate a panel
of V. cholerae RND efflux pump mutants in order to determine the function of VexH in antimicrobial resistance, virulence
factor production, and intestinal colonization. VexH contributed to in vitro antimicrobial resistance and exhibited a broad
substrate specificity that was redundant with the VexB, VexD, and VexK RND efflux pumps. These four efflux pumps were
responsible for in vitro antimicrobial resistance and were required for virulence factor production and intestinal colonization.
Mutation of the VexF and/or VexM efflux pumps did not affect in vitro antimic
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