ArticleInfection and immunity2008
An AraC-type transcriptional regulator encoded on the Enterococcus faecalis pathogenicity island contributes to pathogenesis and intracellular macrophage survival.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Gelatinase regulates the egress of intracellular replicating populations during Enterococcus faecalis infection.PLoS pathogens · 2026Article
- The Role of Livestock Antibiotic Use in Microbiota Dysbiosis and Neuroinflammation.Antibiotics (Basel, Switzerland) · 2025Review
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- CCR2-dependent CX3CR1+ colonic macrophages promoteInfection and immunity · 2024Article
- Review
- BfvR, an AraC-Family Regulator, Controls Biofilm Formation and pH6 Antigen Production in Opposite Ways inFrontiers in cellular and infection microbiology · 2018Article
- Review
- Genome-based characterization of hospital-adaptedNature microbiology · 2016Article
- Overexpression of Enterococcus faecalis elr operon protects from phagocytosis.BMC microbiology · 2015Article
- The Intraperitoneal Transcriptome of the Opportunistic Pathogen Enterococcus faecalis in Mice.PloS one · 2015Article
- Enterococcus faecalis infection activates phosphatidylinositol 3-kinase signaling to block apoptotic cell death in macrophages.Infection and immunity · 2014Article
- A TIR domain protein from E. faecalis attenuates MyD88-mediated signaling and NF-κB activation.PloS one · 2014Article
- Small-molecule inhibitor of the Shigella flexneri master virulence regulator VirF.Infection and immunity · 2013Article
- Identification of a small-molecule inhibitor of bacterial AraC family activators.Journal of biomolecular screening · 2013Article
- Biofilm and planktonic Enterococcus faecalis elicit different responses from host phagocytes in vitro.FEMS immunology and medical microbiology · 2012Article
- The rise of the Enterococcus: beyond vancomycin resistance.Nature reviews. Microbiology · 2012Review
- AsrR is an oxidative stress sensing regulator modulating Enterococcus faecium opportunistic traits, antimicrobial resistance, and pathogenicity.PLoS pathogens · 2012Article
- Transcriptional regulator PerA influences biofilm-associated, platelet binding, and metabolic gene expression in Enterococcus faecalis.PloS one · 2012Article
- SlyA is a transcriptional regulator involved in the virulence of Enterococcus faecalis.Infection and immunity · 2011Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
A gene encoding a putative AraC-type transcriptional regulator was identified on the 153-kb pathogenicity island (PAI) found among virulent Enterococcus faecalis strains. In an effort to understand the function of this regulator, designated PerA (for pathogenicity island-encoded regulator), we first examined the expression of the perA gene in the original PAI strain MMH594 and in an unrelated clinical isolate E99 by reverse transcription-PCR. Interestingly, expression analysis revealed no detectable perA transcript in MMH594, whereas a transcript was observed in strain E99. Nucleotide sequence analysis revealed that this altered expression between the two strains was attributable to the differential location of an IS1191 element within the putative promoter region upstream of the perA gene. In order to determine the role of this putative regulator in E. faecalis pathogenesis, a perA-deficient mutant was created in strain E99, and the wild-type and mutant pair were compared for phenotypic differences. In in vitro biofilm assays, the mutant strain showed a significantly higher level of growth medium-specific biofilm formation compared to the wild type. However, in a murine intraperitoneal infection model, the mutant strain was significantly less pathogenic. The mutant was also attenuated for survival within macrophages in vitro. These findings highlight the importance of PerA as a regulator of biofilm formation and survival within macrophages and is likely a regulator controlling determinants important to pathogenesis.
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