ArticleJournal of microbiology (Seoul, Korea)2015
Functional analysis of Vibrio vulnificus RND efflux pumps homologous to Vibrio cholerae VexAB and VexCD, and to Escherichia coli AcrAB.
Article in Journal of microbiology (Seoul, Korea), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Stress Responses in Pathogenic Vibrios and Their Role in Host and Environmental Survival.Advances in experimental medicine and biology · 2023Article
- Membrane Efflux Pumps of PathogenicMicroorganisms · 2022Review
- TolCV1 Has Multifaceted Roles DuringFrontiers in cellular and infection microbiology · 2021Article
- The mechanisms that regulate Vibrio parahaemolyticus virulence gene expression differ between pathotypes.Microbial genomics · 2018Article
- ATP-Binding Cassette Transporter VcaM from Vibrio cholerae is Dependent on the Outer Membrane Factor Family for Its Function.International journal of molecular sciences · 2018Article
- Survival of the Fittest: How Bacterial Pathogens Utilize Bile To Enhance Infection.Clinical microbiology reviews · 2016Review
- MdsABC-Mediated Pathway for Pathogenicity in Salmonella enterica Serovar Typhimurium.Infection and immunity · 2015Article
- Molecular architecture of the bacterial tripartite multidrug efflux pump focusing on the adaptor bridging model.Journal of microbiology (Seoul, Korea) · 2015Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance-nodulation-division (RND) efflux pumps are associated with multidrug resistance in many gram-negative pathogens. The genome of Vibrio vulnificus encodes 11 putative RND pumps homologous to those of Vibrio cholerae and Escherichia coli. In this study, we analyzed three putative RND efflux pumps, showing homology to V. cholerae VexAB and VexCD and to E. coli AcrAB, for their functional roles in multidrug resistance of V. vulnificus. Deletion of the vexAB homolog resulted in increased susceptibility of V. vulnificus to bile acid, acriflavine, ethidium bromide, and erythromycin, whereas deletion of acrAB homologs rendered V. vulnificus more susceptible to acriflavine only. Deletion of vexCD had no effect on susceptibility of V. vulnificus to these chemicals. Upon exposure to these antibacterial chemicals, expression of tolCV1 and tolCV2, which are putative outer membrane factors of RND efflux pumps, was induced, whereas expression levels of vexAB, vexCD, and acrAB homologs were not significantly changed. Our results show that the V. vulnificus homologs of VexAB largely contributed to in vitro antimicrobial resistance with a broad substrate specificity that was partially redundant with the AcrAB pump homologs.
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