Journal
NATURE COMMUNICATIONS
Volume 13, Issue 1, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41467-022-29919-9
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Funding
- Luxembourg National Research Fund (FNR) [PRIDE/11823097]
- Sinergia grant through the Swiss National Science Foundation [CRSII5_180241]
- European Research Council (ERC) under the European Union [863664]
- Fondation du Pelican de Mie and Pierre Hippert-Faber under Fondation de Luxembourg [E-AGR-0023-10-Z]
- Action LIONS Vaincre le Cancer
- Internal Research Project at the University of Luxembourg [R-AGR-0755-12]
- FNR
- Fondation Cancer Luxembourg [CORE/C20/BM/14591557]
- Club 51 Eislek
- European Research Council (ERC) [863664] Funding Source: European Research Council (ERC)
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Antimicrobial resistance is an ongoing and potential pandemic, and integrons play a key role in mediating this resistance. By studying a murine model, it is found that gut commensals acquire antimicrobial resistance genes after a single antibiotic treatment, and integrons are crucial factors in mediating this resistance.
Antimicrobial resistance represents an ongoing silent pandemic. Here, de Nies et al. show that a single antibiotic treatment leads to resistance in bacteria such as Akkermansia muciniphila and that integrons play a key role in mediating this resistance. The emergence and spread of antimicrobial resistance (AMR) represent an ever-growing healthcare challenge worldwide. Nevertheless, the mechanisms and timescales shaping this resistome remain elusive. Using an antibiotic cocktail administered to a murine model along with a longitudinal sampling strategy, we identify the mechanisms by which gut commensals acquire antimicrobial resistance genes (ARGs) after a single antibiotic course. While most of the resident bacterial populations are depleted due to the treatment, Akkermansia muciniphila and members of the Enterobacteriaceae, Enterococcaceae, and Lactobacillaceae families acquire resistance and remain recalcitrant. We identify specific genes conferring resistance against the antibiotics in the corresponding metagenome-assembled genomes (MAGs) and trace their origins within each genome. Here we show that, while mobile genetic elements (MGEs), including bacteriophages and plasmids, contribute to the spread of ARGs, integrons represent key factors mediating AMR in the antibiotic-treated mice. Our findings suggest that a single course of antibiotics alone may act as the selective sweep driving ARG acquisition and incidence in gut commensals over a single mammalian lifespan.
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