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Gut inflammation can boost horizontal gene transfer between pathogenic and commensal Enterobacteriaceae

2012; National Academy of Sciences; Volume: 109; Issue: 4 Linguagem: Inglês

10.1073/pnas.1113246109

1091-6490

Bärbel Stecher, Rémy Denzler, Lisa Maier, Florian Bernet, Mandy Sanders, Derek Pickard, Manja Barthel, Astrid M. Westendorf, Karen A. Krogfelt, Alan W. Walker, Martin Ackermann, Ulrich Dobrindt, Nicholas R. Thomson, Wolf‐Dietrich Hardt,

Viral gastroenteritis research and epidemiology

The mammalian gut harbors a dense microbial community interacting in multiple ways, including horizontal gene transfer (HGT). Pangenome analyses established particularly high levels of genetic flux between Gram-negative Enterobacteriaceae . However, the mechanisms fostering intraenterobacterial HGT are incompletely understood. Using a mouse colitis model, we found that Salmonella -inflicted enteropathy elicits parallel blooms of the pathogen and of resident commensal Escherichia coli . These blooms boosted conjugative HGT of the colicin-plasmid p2 from Salmonella enterica serovar Typhimurium to E. coli . Transconjugation efficiencies of ∼100% in vivo were attributable to high intrinsic p2-transfer rates. Plasmid-encoded fitness benefits contributed little. Under normal conditions, HGT was blocked by the commensal microbiota inhibiting contact-dependent conjugation between Enterobacteriaceae . Our data show that pathogen-driven inflammatory responses in the gut can generate transient enterobacterial blooms in which conjugative transfer occurs at unprecedented rates. These blooms may favor reassortment of plasmid-encoded genes between pathogens and commensals fostering the spread of fitness-, virulence-, and antibiotic-resistance determinants.