Spatial and temporal modulation of enterotoxigenic E. coli H10407 pathogenesis and interplay with microbiota in human gut models

BMC Biology

Kim De Paepe¹  Jana De Bodt¹  Tom Van de Wiele¹  Nathalie Ballet²  Wessam Galia³  Françoise Leriche⁴  Sylvain Denis⁵  Sandrine Chalancon⁵  Stéphanie Blanquet-Diot⁵  Monique Alric⁵  Charlène Roussel⁶ 

[1] CMET, Center for Microbial Ecology and Technology, Department of Biotechnology, Faculty of Bioscience Engineering, Ghent University, Ghent, Belgium;Lesaffre International, Lesaffre Group, Marcq-en-Baroeul, France;UMR 5557 Microbial Ecology, Research Group on Bacterial Opportunistic Pathogens and Environment, CNRS, VetAgro Sup, Lyon, France;Unité de recherche Fromagère, VetAgro Sup, Lempdes, France;Université Clermont Auvergne, UMR UCA-INRA 454 MEDIS, Microbiology Digestive Environment and Health, Clermont-Ferrand, France;Université Clermont Auvergne, UMR UCA-INRA 454 MEDIS, Microbiology Digestive Environment and Health, Clermont-Ferrand, France;CMET, Center for Microbial Ecology and Technology, Department of Biotechnology, Faculty of Bioscience Engineering, Ghent University, Ghent, Belgium;

关键词: ETEC pathogenesis;    Survival;    Virulence;    Gut microbes;    Digestive in vitro systems;   

DOI  :  10.1186/s12915-020-00860-x

来源: Springer

【 摘 要 】

BackgroundEnterotoxigenic Escherichia coli (ETEC) substantially contributes to the burden of diarrheal illnesses in developing countries. With the use of complementary in vitro models of the human digestive environment, TNO gastrointestinal model (TIM-1), and Mucosal Simulator of the Human Intestinal Microbial Ecosystem (M-SHIME), we provided the first detailed report on the spatial-temporal modulation of ETEC H10407 survival, virulence, and its interplay with gut microbiota. These systems integrate the main physicochemical parameters of the human upper digestion (TIM-1) and simulate the ileum vs ascending colon microbial communities and luminal vs mucosal microenvironments, captured from six fecal donors (M-SHIME).ResultsA loss of ETEC viability was noticed upon gastric digestion, while a growth renewal was found at the end of jejunal and ileal digestion. The remarkable ETEC mucosal attachment helped to maintain luminal concentrations above 6 log10 mL−1 in the ileum and ascending colon up to 5 days post-infection. Seven ETEC virulence genes were monitored. Most of them were switched on in the stomach and switched off in the TIM-1 ileal effluents and in a late post-infectious stage in the M-SHIME ascending colon. No heat-labile enterotoxin production was measured in the stomach in contrast to the ileum and ascending colon. Using 16S rRNA gene-based amplicon sequencing, ETEC infection modulated the microbial community structure of the ileum mucus and ascending colon lumen.ConclusionsThis study provides a better understanding of the interplay between ETEC and gastrointestinal cues and may serve to complete knowledge on ETEC pathogenesis and inspire novel prophylactic strategies for diarrheal diseases.

【 授权许可】

CC BY