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• W2143111495 abstract "The authors develop a mouse model of Enterococcus faecalis colonization to show that enterococci harbouring the bacteriocin-expressing plasmid pPD1 replace indigenous enterococci and have the ability to transfer the plasmid to other enterococci, which enhances the stability of the bacteriocin-expressing bacteria in the gut; this result suggests a therapeutic approach that leverages niche-specificity to eliminate antibiotic-resistant bacteria from infected individuals. Enterococcus faecalis is a normal gut bacterium and is usually harmless, but it can cause a variety of hospital-acquired infections in which its acquisition of antibiotic resistance makes it hard to treat. Nita Salzman and colleagues develop a mouse model of E. faecalis infection and use it to show that enterococci harbouring the bacteriocin-expressing plasmid pPD1 replace indigenous enterococci and have the ability to transfer the plasmid to other enterococci, thereby enhancing the stability of the bacteriocin-expressing bacteria in the gut. However, colonization by a strain in which the plasmid was not passed on resulted in clearance of other enterococci strains from the gut — including those resistant to the antibiotic vancomycin. This result suggests a way of using bacteriocin-producing bacteria as targeted therapeutics designed to clear competing multidrug-resistant strains from infected individuals. Enterococcus faecalis is both a common commensal of the human gastrointestinal tract and a leading cause of hospital-acquired infections1. Systemic infections with multidrug-resistant enterococci occur subsequent to gastrointestinal colonization2. Preventing colonization by multidrug-resistant E. faecalis could therefore be a valuable approach towards limiting infection. However, little is known about the mechanisms E. faecalis uses to colonize and compete for stable gastrointestinal niches. Pheromone-responsive conjugative plasmids encoding bacteriocins are common among enterococcal strains3 and could modulate niche competition among enterococci or between enterococci and the intestinal microbiota. We developed a model of colonization of the mouse gut with E. faecalis, without disrupting the microbiota, to evaluate the role of the conjugative plasmid pPD1 expressing bacteriocin 21 (ref. 4) in enterococcal colonization. Here we show that E. faecalis harbouring pPD1 replaces indigenous enterococci and outcompetes E. faecalis lacking pPD1. Furthermore, in the intestine, pPD1 is transferred to other E. faecalis strains by conjugation, enhancing their survival. Colonization with an E. faecalis strain carrying a conjugation-defective pPD1 mutant subsequently resulted in clearance of vancomycin-resistant enterococci, without plasmid transfer. Therefore, bacteriocin expression by commensal bacteria can influence niche competition in the gastrointestinal tract, and bacteriocins, delivered by commensals that occupy a precise intestinal bacterial niche, may be an effective therapeutic approach to specifically eliminate intestinal colonization by multidrug-resistant bacteria, without profound disruption of the indigenous microbiota." @default.
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• W2143111495 date "2015-10-01" @default.
• W2143111495 modified "2023-10-15" @default.
• W2143111495 title "Bacteriocin production augments niche competition by enterococci in the mammalian gastrointestinal tract" @default.
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• W2143111495 doi "https://doi.org/10.1038/nature15524" @default.
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