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

Enterococcus 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. faecal...

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Autores principales: Li, Farry J., Palmer, Kelli L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Society for Microbiology 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5971576/
https://www.ncbi.nlm.nih.gov/pubmed/29610200
http://dx.doi.org/10.1128/AAC.00267-18
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author Li, Farry J.
Palmer, Kelli L.
author_facet Li, Farry J.
Palmer, Kelli L.
author_sort Li, Farry J.
collection PubMed
description Enterococcus 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.
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spelling pubmed-59715762018-05-31 EfrEF and the Transcription Regulator ChlR Are Required for Chlorhexidine Stress Response in Enterococcus faecalis V583 Li, Farry J. Palmer, Kelli L. Antimicrob Agents Chemother Mechanisms of Resistance Enterococcus 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. American Society for Microbiology 2018-05-25 /pmc/articles/PMC5971576/ /pubmed/29610200 http://dx.doi.org/10.1128/AAC.00267-18 Text en Copyright © 2018 Li and Palmer. https://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Mechanisms of Resistance
Li, Farry J.
Palmer, Kelli L.
EfrEF and the Transcription Regulator ChlR Are Required for Chlorhexidine Stress Response in Enterococcus faecalis V583
title EfrEF and the Transcription Regulator ChlR Are Required for Chlorhexidine Stress Response in Enterococcus faecalis V583
title_full EfrEF and the Transcription Regulator ChlR Are Required for Chlorhexidine Stress Response in Enterococcus faecalis V583
title_fullStr EfrEF and the Transcription Regulator ChlR Are Required for Chlorhexidine Stress Response in Enterococcus faecalis V583
title_full_unstemmed EfrEF and the Transcription Regulator ChlR Are Required for Chlorhexidine Stress Response in Enterococcus faecalis V583
title_short EfrEF and the Transcription Regulator ChlR Are Required for Chlorhexidine Stress Response in Enterococcus faecalis V583
title_sort efref and the transcription regulator chlr are required for chlorhexidine stress response in enterococcus faecalis v583
topic Mechanisms of Resistance
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5971576/
https://www.ncbi.nlm.nih.gov/pubmed/29610200
http://dx.doi.org/10.1128/AAC.00267-18
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