[en] The change of dietary habits in Western societies, including reduced consumption of fiber, is linked to alterations in gut microbial ecology. Nevertheless, mechanistic connections between diet-induced microbiota changes that affect colonization resistance and enteric pathogen susceptibility are still emerging. We sought to investigate how a diet devoid of soluble plant fibers impacts the structure and function of a conventional gut microbiota in specific-pathogen-free (SPF) mice and how such changes alter susceptibility to a rodent enteric pathogen. We show that absence of dietary fiber intake leads to shifts in the abundances of specific taxa, microbiome-mediated erosion of the colonic mucus barrier, a reduction of intestinal barrier-promoting short-chain fatty acids, and increases in markers of mucosal barrier integrity disruption. Importantly, our results highlight that these low-fiber diet-induced changes in the gut microbial ecology collectively contribute to a lethal colitis by the mucosal pathogen Citrobacter rodentium, which is used as a mouse model for enteropathogenic and enterohemorrhagic Escherichia coli (EPEC and EHEC, respectively). Our study indicates that modern, low-fiber Western-style diets might make individuals more prone to infection by enteric pathogens via the disruption of mucosal barrier integrity by diet-driven changes in the gut microbiota, illustrating possible implications for EPEC and EHEC infections.
Disciplines :
Immunology & infectious disease
Author, co-author :
Neumann, Mareike; Department of Infection and Immunity, Luxembourg Institute of Health, Esch-sur-Alzette, Luxembourg ; Faculty of Science, Technology and Medicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg
Steimle, Alex; Department of Infection and Immunity, Luxembourg Institute of Health, Esch-sur-Alzette, Luxembourg
Grant, Erica T; Department of Infection and Immunity, Luxembourg Institute of Health, Esch-sur-Alzette, Luxembourg ; Faculty of Science, Technology and Medicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg
Wolter, Mathis; Department of Infection and Immunity, Luxembourg Institute of Health, Esch-sur-Alzette, Luxembourg ; Faculty of Science, Technology and Medicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg
Parrish, Amy; Department of Infection and Immunity, Luxembourg Institute of Health, Esch-sur-Alzette, Luxembourg ; Faculty of Science, Technology and Medicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg
Willieme, Stéphanie; Department of Infection and Immunity, Luxembourg Institute of Health, Esch-sur-Alzette, Luxembourg
BRENNER, Dirk ; University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB) > Immunology and Genetics ; Department of Infection and Immunity, Luxembourg Institute of Health, Esch-sur-Alzette, Luxembourg ; Odense Research Center for Anaphylaxis, Department of Dermatology and Allergy Center, Odense University Hospital, University of Southern Denmark, Odense, Denmark
Martens, Eric C; Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, USA
Desai, Mahesh S ; Department of Infection and Immunity, Luxembourg Institute of Health, Esch-sur-Alzette, Luxembourg ; Odense Research Center for Anaphylaxis, Department of Dermatology and Allergy Center, Odense University Hospital, University of Southern Denmark, Odense, Denmark
External co-authors :
yes
Language :
English
Title :
Deprivation of dietary fiber in specific-pathogen-free mice promotes susceptibility to the intestinal mucosal pathogen Citrobacter rodentium.
National Institutes of Health Fonds National de la Recherche Luxembourg Fonds National de la Recherche Luxembourg Fonds National de la Recherche Luxembourg Fonds National de la Recherche Luxembourg Fonds National de la Recherche Luxembourg
Funding text :
Work in the authors’ laboratory was supported by the following grants to M.S.D.: Luxembourg National Research Fund (FNR) CORE grants (C15/BM/10318186 and C18/BM/12585940). M.N. and A.P. and were supported by the FNR AFR bilateral grant (15/11228353) and FNR AFR individual grant (11602973), respectively. E.T.G. was supported by the FNR PRIDE grant (17/11823097) and the Fondation du Pélican de Mie et Pierre Hippert‐Faber under the aegis of the Fondation de Luxembourg. D.B. is supported by the FNR-ATTRACT program (A14/BM/7632103). E.C.M. was supported by grants from the US National Institutes of Health (DK118024 and DK125445).Work in the authors? laboratory was supported by the following grants to M.S.D.: Luxembourg National Research Fund (FNR) CORE grants (C15/BM/10318186 and C18/BM/12585940). M.N. and A.P. and were supported by the FNR AFR bilateral grant (15/11228353) and FNR AFR individual grant (11602973), respectively. E.T.G. was supported by the FNR PRIDE grant (17/11823097) and the Fondation du P?lican de Mie et Pierre Hippert?Faber under the aegis of the Fondation de Luxembourg. D.B. is supported by the FNR-ATTRACT program (A14/BM/7632103). E.C.M. was supported by grants from the US National Institutes of Health (DK118024 and DK125445).
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