ArticleScientific reports2018
Exploration of the role of the virulence factor ElrA during Enterococcus faecalis cell infection.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Article
- Highly Alkaline-ResistantMicroorganisms · 2025Article
- Review
- DUF916 and DUF3324 in the WxL protein cluster bind to WxL and link bacterial and host surfaces.Protein science : a publication of the Protein Society · 2023Article
- Prevalence ofPathogens (Basel, Switzerland) · 2023Article
- Bioinformatic analysis of WxL domain proteins.Saudi journal of biological sciences · 2023Article
- Vancomycin-variable enterococci in sheep and cattle isolates and whole-genome sequencing analysis of isolates harboringIranian journal of veterinary research · 2023Article
- Involvement of Chromosomally Encoded Homologs of the RRNPP Protein Family in Enterococcus faecalis Biofilm Formation and Urinary Tract Infection Pathogenesis.Journal of bacteriology · 2020Article
- Genetics of Lactococci.Microbiology spectrum · 2019Review
- Intestinal translocation of enterococci requires a threshold level of enterococcal overgrowth in the lumen.Scientific reports · 2019Article
- The unforeseen intracellular lifestyle ofGut microbesArticle
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Authors and funding
11 authors.
Funding
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Abstract
Enterococcus faecalis, an organism generally not pathogenic for healthy humans, has the potential to cause disease in susceptible hosts. While it seems to be equipped to interact with and circumvent host immune defense, most of the molecular and cellular mechanisms underlying the enterococcal infectious process remain elusive. Here, we investigated the role of the Enterococcal Leucine Rich protein A (ElrA), an internalin-like protein of E. faecalis also known as a virulence factor. ElrA was previously shown to prevent adhesion to macrophages. We show that ElrA does not inhibit the basic phagocytic process, but is able to prevent sensing and migration of macrophages toward E. faecalis. Presence or absence of FHL2, a eukaryotic partner of ElrA, does not affect the ElrA-dependent mechanism preventing macrophage migration. However, we highlight a partial contribution of FHL2 in ElrA-mediated virulence in vivo. Our results indicate that ElrA plays at least a dual role of which anti-phagocytic activity may contribute to dissemination of extracellular E. faecalis during infection.
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