Cited by 539Gut microbiota and healthInflammatory Bowel DiseaseGastrointestinal motility and disorders

Western diet induces dysbiosis with increased E coli in CEABAC10 mice , alters host barrier function favouring AIEC colonisation

Martinez-Medina, Margarita, Denizot, Jérémy, Dreux, Nicolas, Robin, Frédéric, Billard, Elisabeth, Bonnet, Richard, Darfeuille-Michaud, Arlette, Barnich, Nicolas·2014·Gut

Abstract

OBJECTIVE: Western diet is a risk factor for Crohn's disease (CD). Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) is abnormally expressed in CD patients. This allows adherent-invasive Escherichia coli (AIEC) to colonise the gut mucosa and leads to inflammation. We assessed the effects of a high fat/high sugar (HF/HS) Western diet on gut microbiota composition, barrier integrity and susceptibility to infection in transgenic CEABAC10 mice expressing human CEACAMs. DESIGN: Colonic microbiota composition and susceptibility of CEABAC10 mice to AIEC LF82 bacteria infection were determined in mice fed a conventional or HF/HS diet. Barrier function and inflammatory response were assessed by studying intestinal permeability, tight junction protein and mucin expression and localisation, and by determining histological score and levels of cytokine release. RESULTS: HF/HS diet led to dysbiosis in WT and transgenic CEABAC10 mice, with a particular increase in E coli population in HF/HS-fed CEABAC10 mice. These mice showed decreased mucus layer thickness, increased intestinal permeability, induction of Nod2 and Tlr5 gene transcription, and increased TNFα secretion. These modifications led to a higher ability of AIEC bacteria to colonise the gut mucosa and to induce inflammation. CONCLUSIONS: Western diet induces changes in gut microbiota composition, alters host homeostasis and promotes AIEC gut colonisation in genetically susceptible mice. These results support the multifactorial aetiology of CD and highlight the importance of diet in CD pathogenesis.

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Crossref · 10.1136/gutjnl-2012-304119

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Authors
Martinez-Medina, M., Denizot, J., Dreux, N., Robin, F., Billard, E., Bonnet, R., Darfeuille-Michaud, A., & Barnich, N.
Affiliations
  • Clermont Université, ‘Microbe intestin inflammation et Susceptibilité de l'Hôte’, UMR1071 Inserm/Université d'Auvergne M2iSH, Clermont-Ferrand, France
  • Inserm (FR)
Corresponding author
Barnich, Nicolas
Venue
Gut
Publisher
BMJ
Published
2013-04-18
Volume
63
Issue
1
Pages
116-124
ISSN
  • 0017-5749 (ISSN-L)
  • 1468-3288
OpenAlex
W2097855460
Cited by
539
References
51
Citations by year
2026: 16 · 2025: 40 · 2024: 44 · 2023: 47 · 2022: 58 · 2021: 54 · 2020: 74 · 2019: 52 · 2018: 33 · 2017: 31 · 2016: 22 · 2015: 29 · 2014: 32 · 2013: 6
FWCI
13.30
Type
journal article
Language
en
Open access
closed
Locations
  • Gut (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
  • HighWire Press Open Archive (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
  • Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
Keywords
Western diet, high-fat high-sugar diet, Crohn's disease, gut dysbiosis, adherent-invasive Escherichia coli, CEACAM6, intestinal barrier function, intestinal permeability, mucus layer, NOD2, TLR5, TNF-α, gut microbiota, diet and inflammation
MeSH terms
Animals, Colon, Crohn Disease, Escherichia coli, Escherichia coli Infections, Female, Homeostasis, Intestinal Mucosa, Mice, Inbred C57BL, Mice, Transgenic, Biomarkers, Cell Adhesion Molecules, Cytokines, Dietary Sucrose, Genetic Predisposition to Disease, Mice, Host-Pathogen Interactions, Diet, High-Fat, Microbiota, Dysbiosis

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