@article{51f3da437ead4a60a24c69d12a8ead91,
title = "Deprivation of dietary fiber in specific-pathogen-free mice promotes susceptibility to the intestinal mucosal pathogen Citrobacter rodentium",
abstract = "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.",
keywords = "Microbiome, SPF mice, citrobacter rodentium, dietary fiber, mucin, mucus layer",
author = "Mareike Neumann and Alex Steimle and Erica Grant and Mathis Wolter and Amy Parrish and St{\'e}phanie Willieme and Dirk Brenner and Martens, {Eric C.} and Desai, {Mahesh S.}",
note = "Funding Information: Work in the authors{\textquoteright} 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{\'e}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). Funding Information: 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). Publisher Copyright: {\textcopyright} 2021 The Author(s). Published with license by Taylor & Francis Group, LLC.",
year = "2021",
month = sep,
day = "18",
doi = "10.1080/19490976.2021.1966263",
language = "English",
volume = "13",
pages = "1966263",
journal = "Gut Microbes",
issn = "1949-0976",
publisher = "Landes Bioscience",
number = "1",
}