Abstract
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.
Original language | English |
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Pages (from-to) | 1269-1274 |
Number of pages | 6 |
Journal | PNAS |
Volume | 109 |
Issue number | 4 |
DOIs | |
Publication status | Published - 24 Jan 2012 |
Keywords
- animals
- bacteriocin plasmids
- base sequence
- biological evolution
- colitis
- computational biology
- DNA primers
- enterobacteriaceae
- Escherichia coli
- gene transfer, horizontal
- mice
- molecular sequence data
- oligonucleotide array sequence analysis
- phylogeny
- RNA, ribosomal, 16S
- Salmonella typhimurium
- sequence alignment
- sequence analysis, DNA