| Literature DB >> 24971581 |
Delphine Payros1, Thomas Secher2, Michèle Boury2, Camille Brehin3, Sandrine Ménard4, Christel Salvador-Cartier4, Gabriel Cuevas-Ramos2, Claude Watrin2, Ingrid Marcq5, Jean-Philippe Nougayrède2, Damien Dubois3, Antoine Bedu6, Fabien Garnier7, Olivier Clermont8, Erick Denamur8, Pascale Plaisancié9, Vassilia Theodorou4, Jean Fioramonti4, Maïwenn Olier1, Eric Oswald3.
Abstract
The neonatal gut is rapidly colonized by a newly dominant group of commensal Escherichia coli strains among which a large proportion produces a genotoxin called colibactin. In order to analyze the short- and long-term effects resulting from such evolution, we developed a rat model mimicking the natural transmission of E. coli from mothers to neonates. Genotoxic and non-genotoxic E. coli strains were equally transmitted to the offspring and stably colonized the gut across generations. DNA damage was only detected in neonates colonized with genotoxic E. coli strains. Signs of genotoxic stress such as anaphase bridges, higher occurrence of crypt fission and accelerated renewal of the mature epithelium were detected at adulthood. In addition, we observed alterations of secretory cell populations and gut epithelial barrier. Our findings illustrate how critical is the genotype of E. coli strains acquired at birth for gut homeostasis at adulthood.Entities:
Keywords: Escherichia coli; colibactin; epithelial differentiation; epithelial proliferation; genotoxicity; gut; intestinal barrier; neonate
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Year: 2014 PMID: 24971581 PMCID: PMC4153768 DOI: 10.4161/gmic.28932
Source DB: PubMed Journal: Gut Microbes ISSN: 1949-0976