EfrEF and the Transcription Regulator ChIR Are Required for Chlorhexidine Stress Response in Enterococcus faecalis V583

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dc.contributor.authorLi, Farry J.
dc.contributor.authorPalmer, Kelli L.
dc.contributor.utdAuthorLi, Farry J.
dc.contributor.utdAuthorPalmer, Kelli L.
dc.date.accessioned2019-06-28T18:13:35Z
dc.date.available2019-06-28T18:13:35Z
dc.date.created2018-05-25
dc.description.abstractEnterococcus faecalis is an opportunistic pathogen and leading cause of health care-associated infections. Daily chlorhexidine gluconate (CHG) bathing of patients is generally regarded as an effective strategy to reduce the occurrence of health care-associated infections. It is likely that E. faecalis is frequently exposed to inhibitory and subinhibitory concentrations of CHG in clinical settings. The goal of this study was to investigate how the vancomycin-resistant strain E. faecalis V583 transcriptionally responds to and tolerates stress from CHG. We used transcriptome (microarray) analysis to identify genes upregulated by E. faecalis V583 in response to CHG. The genes efrE (EF2226) and efrF (EF2227), encoding a heterodimeric ABC transport system, were the most highly upregulated genes. efrEF expression was induced by CHG at concentrations several 2-fold dilutions below the MIC. Deletion of efrEF increased E. faecalis V583 susceptibility to CHG. We found that ChlR, a MerR-like regulator encoded by a sequence upstream of efrEF, mediated the CHG-dependent upregulation of efrEF, and deletion of chlR also increased chlorhexidine susceptibility. Overall, our study gives insight into E. faecalis stress responses to a commonly used antiseptic.
dc.description.departmentSchool of Natural Sciences and Mathematics
dc.identifier.bibliographicCitationLi, F. J., and K. L. Palmer. 2018. "EfrEF and the transcription regulator chIR are required for chlorhexidine stress response in enterococcus faecalis V583." Antimicrobial Agents and Chemotherapy 62(6): art. e00267-18, doi:10.1128/AAC.00267-18
dc.identifier.issn0066-4804
dc.identifier.issue6
dc.identifier.urihttps://hdl.handle.net/10735.1/6626
dc.identifier.volume62
dc.language.isoen
dc.publisherAmerican Society for Microbiology
dc.relation.urihttp://dx.doi.org/10.1128/AAC.00267-18
dc.rightsCC BY 4.0 (Attribution)
dc.rights©2018 The Authors
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.source.journalAntimicrobial Agents and Chemotherapy
dc.subjectChlorhexidine
dc.subjectEnterococcus faecalis
dc.subjectBacterial proteins
dc.subjectChlorhexidine gluconate
dc.subjectPentamidine
dc.subjectBacterial growth
dc.subjectDisease susceptibility
dc.subjectGene Deletion
dc.subjectGene expression
dc.subjectMicroarray Analysis
dc.subjectMicrobial Sensitivity Tests
dc.subjectPromoter Regions, Genetic
dc.subjectUp-Regulation
dc.subjectVancomycin-Resistant Enterococci
dc.titleEfrEF and the Transcription Regulator ChIR Are Required for Chlorhexidine Stress Response in Enterococcus faecalis V583
dc.type.genrearticle

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