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

作者：Stecher Baerbel^*; Denzler Remy; Maier Lisa; Bernet Florian; Sanders Mandy J; Pickard Derek J; Barthel Manja; Westendorf Astrid M; Krogfelt Karen A; Walker Alan W; Ackermann Martin; Dobrindt Ulrich; Thomson Nicholas R; Hardt Wolf Dietrich

来源：Proceedings of the National Academy of Sciences, 2012, 109(4): 1269-1274.

DOI：10.1073/pnas.1113246109

• bacterial evolution
• hospital-acquired infection
• mucosal immune response
• plasmid spread

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 similar to 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.

• 出版日期2012-1-24
• 单位河北医科大学