ArticlePLoS pathogens2015
Phage-mediated dispersal of biofilm and distribution of bacterial virulence genes is induced by quorum sensing.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed.
- Participation of the Transcriptional Regulator Fur in Modulating Biofilm Formation of the Salmonid PathogenInternational journal of molecular sciences · 2026Article
- Biofilm dispersion inbioRxiv : the preprint server for biology · 2026Article
- LuxS/AI-2 regulates phoP/phoQ by a non-canonical mechanism to enhance acid stress survival in Salmonella Typhimurium.PLoS pathogens · 2026Article
- Effects of bacteriophages on gut microbiome functionality.Gut microbes · 2025Review
- Natural products influence bacteriophage infectivity.Natural product reports · 2025Review
- Cell differentiation, aging, and death in spatially organized yeast communities: mechanisms and consequences.Cell death and differentiation · 2025Review
- A φSa3int (NM3) Prophage Domestication inMedComm · 2025Article
- The Role of Quorum Sensing in Phage Lifecycle Decision: A Switch Between Lytic and Lysogenic Pathways.Viruses · 2025Review
- Intestinal dysbiosis associated with non-nutritive sweeteners intake: an effect without a cause?Frontiers in nutrition · 2025Review
- Review
- Prophage induction can facilitate the in vitro dispersal of multicellular Streptomyces structures.PLoS biology · 2024Article
- The LuxO-OpaR quorum-sensing cascade differentially controls Vibriophage VP882 lysis-lysogeny decision making in liquid and on surfaces.PLoS genetics · 2024Article
- Enterococcal quorum-controlled protease alters phage infection.bioRxiv : the preprint server for biology · 2024Article
- Improving phage therapy by evasion of phage resistance mechanisms.JAC-antimicrobial resistance · 2024Review
- Enterococcal quorum-controlled protease alters phage infection.FEMS microbes · 2024Article
- Natural silencing of quorum-sensing activity protects Vibrio parahaemolyticus from lysis by an autoinducer-detecting phage.PLoS genetics · 2023Article
- Natural Silencing of Quorum-Sensing Activity ProtectsbioRxiv : the preprint server for biology · 2023Article
- Signals triggering prophage induction in the gut microbiota.Molecular microbiology · 2022Review
- How does Quorum Sensing of Intestinal Bacteria Affect Our Health and Mental Status?Microorganisms · 2022Review
- Homocysteine and Inflammatory Cytokines in the Clinical Assessment of Infection in Venous Leg Ulcers.Antibiotics (Basel, Switzerland) · 2022Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The microbiome and the phage meta-genome within the human gut are influenced by antibiotic treatments. Identifying a novel mechanism, here we demonstrate that bacteria use the universal communication molecule AI-2 to induce virulence genes and transfer them via phage release. High concentrations (i.e. 100 μM) of AI-2 promote dispersal of bacteria from already established biofilms, and is associated with release of phages capable of infecting other bacteria. Enterococcus faecalis V583ΔABC harbours 7 prophages in its genome, and a mutant deficient in one of these prophages (i.e. prophage 5) showed a greatly reduced dispersal of biofilm. Infection of a probiotic E. faecalis strain without lytic prophages with prophage 5 resulted in increased biofilm formation and also in biofilm dispersal upon induction with AI-2. Infection of the probiotic E. faecalis strain with phage-containing supernatants released through AI-2 from E. faecalis V583ΔABC resulted in a strong increase in pathogenicity of this strain. The polylysogenic probiotic strain was also more virulent in a mouse sepsis model and a rat endocarditis model. Both AI-2 and ciprofloxacin lead to phage release, indicating that conditions in the gastrointestinal tract of hospitalized patients treated with antibiotics might lead to distribution of virulence genes to apathogenic enterococci and possibly also to other commensals or even to beneficial probiotic strains.
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