ArticlePloS one2014
Cell-wall glycolipid mutations and their effects on virulence of E. faecalis in a rat model of infective endocarditis.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Loss of Fsr quorum sensing promotes biofilm formation and worsens outcomes in enterococcal infective endocarditis.Nature communications · 2026Article
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- Transcriptome analysis reveals the molecular mechanism of γ-linolenic acid eradicating the biofilm of vancomycin-resistantFrontiers in cellular and infection microbiology · 2025Article
- Enterococcal-host interactions in the gastrointestinal tract and beyond.FEMS microbes · 2024Review
- YajC, a predicted membrane protein, promotesFEMS microbes · 2024Article
- Anti-biofilm Approach in Infective Endocarditis Exposes New Treatment Strategies for Improved Outcome.Frontiers in cell and developmental biology · 2021Review
- Comparative genomics of globalMicrobial genomics · 2020Article
- Detection and characterization of bacterial polysaccharides in drug-resistant enterococci.Glycoconjugate journal · 2019Article
- Review
- Virulence Factors Associated withThe open microbiology journal · 2017Review
- Comprehensive molecular, genomic and phenotypic analysis of a major clone of Enterococcus faecalis MLST ST40.BMC genomics · 2015Article
- Phage-mediated dispersal of biofilm and distribution of bacterial virulence genes is induced by quorum sensing.PLoS pathogens · 2015Article
- Isolation of highly active monoclonal antibodies against multiresistant gram-positive bacteria.PloS one · 2015Article
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterococci are among the major pathogens implicated in cardiac infections and biofilm formation. E. faecalis has been shown to play an important role in infectious endocarditis. Several distinct mechanisms for biofilm formation have been identified in E. faecalis. Our group has previously characterized two distinct bacterial glucosyltransferases playing key roles in the production of the major cell wall glycolipids and leading to reduced biofilm production. To assess if this mechanism is involved in the pathogenesis of enterococcal endocarditis we compared the wild-type strain of E. faecalis 12030 with two mutants in gene EF2891 and EF2890 respectively in a rat model of infective endocarditis. The results showed less endocarditic lesions and reduced colony counts per vegetation in the two mutants. indicating that the modification of bacterial surface lipids results in significantly reduced virulence in infective endocarditis. These results underscore the important role of biofilm formation in the pathogenicity of enterococcal endocarditis and may indicate an interesting target for novel therapeutic strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.