Dataset Information

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

ABSTRACT: 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.

SUBMITTER: Li FJ

PROVIDER: S-EPMC5971576 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature

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

Li Farry J FJ Palmer Kelli L KL

Antimicrobial agents and chemotherapy 20180525 6

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. f ...[more]

PMID: 29610200

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Project description:Enterococcus faecalis is a robust bacterium, which is able to survive in and adapt to hostile environments such as the urinary tract and bladder. In this label-free quantitative proteomic study based on MaxQuant LFQ algorithms, we identified 127 proteins present in the secretome of the clinical vancomycin-resistant isolate E. faecalis V583 and we compared proteins secreted in the initial phase of cultivation in urine with the secretome during cultivation in standard laboratory medium, 2xYT. Of the 54 identified proteins predicted to be secreted, six were exclusively found after cultivation in urine including the virulence factor EfaA ("endocarditis specific antigen") and its homologue EF0577 ("adhesion lipoprotein"). These two proteins are both involved in manganese transport, known to be an important determinant of colonization and infection, and may additionally function as adhesins. Other detected urine-specific proteins are involved in peptide transport (EF0063 and EF3106) and protease inhibition (EF3054). In addition, we found an uncharacterized protein (EF0764), which had not previously been linked to the adaptation of V583 to a urine environment, and which is unique to E. faecalis. Proteins found in both environments included a histone-like protein, EF1550, that was up-regulated during cultivation in urine and that has a homologue in streptococci (HlpA) known to be involved in bacterial adhesion to host cells. Up-regulated secreted proteins included autolysins. These results from secretome analyses are largely compatible with previously published data from transcriptomics studies. All in all, the present data indicate that transport, in particular metal transport, adhesion, cell wall remodelling and the unknown function carried out by the unique EF0764 are important for enterococcal adaptation to the urine environment. These results provide a basis for a more targeted exploration of novel proteins involved in the adaptability and pathogenicity of E. faecalis.

Dataset Information

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

Publications

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

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