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Diet and specific microbial exposure trigger features of environmental enteropathy in a novel murine model

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Listed:
  • Eric M. Brown

    (University of British Columbia
    Michael Smith Laboratories, University of British Columbia)

  • Marta Wlodarska

    (University of British Columbia
    Michael Smith Laboratories, University of British Columbia)

  • Benjamin P. Willing

    (Food and Nutritional Science, University of Alberta)

  • Pascale Vonaesch

    (Molecular Microbial Pathogenesis Unit, Institut Pasteur)

  • Jun Han

    (The UVic-Genome British Columbia Proteomics Centre, University of Victoria)

  • Lisa A. Reynolds

    (Michael Smith Laboratories, University of British Columbia)

  • Marie-Claire Arrieta

    (Michael Smith Laboratories, University of British Columbia)

  • Marco Uhrig

    (University of British Columbia)

  • Roland Scholz

    (Michael Smith Laboratories, University of British Columbia)

  • Oswaldo Partida

    (Michael Smith Laboratories, University of British Columbia)

  • Christoph H. Borchers

    (The UVic-Genome British Columbia Proteomics Centre, University of Victoria
    University of Victoria)

  • Philippe J. Sansonetti

    (Molecular Microbial Pathogenesis Unit, Institut Pasteur)

  • B. Brett Finlay

    (University of British Columbia
    Michael Smith Laboratories, University of British Columbia
    University of British Columbia)

Abstract

Environmental enteropathy (EE) is a subclinical chronic inflammatory disease of the small intestine and has a profound impact on the persistence of childhood malnutrition worldwide. However, the aetiology of the disease remains unknown and no animal model exists to date, the creation of which would aid in understanding this complex disease. Here we demonstrate that early-life consumption of a moderately malnourished diet, in combination with iterative oral exposure to commensal Bacteroidales species and Escherichia coli, remodels the murine small intestine to resemble features of EE observed in humans. We further report the profound changes that malnutrition imparts on the small intestinal microbiota, metabolite and intraepithelial lymphocyte composition, along with the susceptibility to enteric infection. Our findings provide evidence indicating that both diet and microbes combine to contribute to the aetiology of EE, and describe a novel murine model that can be used to elucidate the mechanisms behind this understudied disease.

Suggested Citation

  • Eric M. Brown & Marta Wlodarska & Benjamin P. Willing & Pascale Vonaesch & Jun Han & Lisa A. Reynolds & Marie-Claire Arrieta & Marco Uhrig & Roland Scholz & Oswaldo Partida & Christoph H. Borchers & P, 2015. "Diet and specific microbial exposure trigger features of environmental enteropathy in a novel murine model," Nature Communications, Nature, vol. 6(1), pages 1-16, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8806
    DOI: 10.1038/ncomms8806
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    Cited by:

    1. K. E. Huus & T. T. Hoang & A. Creus-Cuadros & M. Cirstea & S. L. Vogt & K. Knuff-Janzen & P. J. Sansonetti & P. Vonaesch & B. B. Finlay, 2021. "Cross-feeding between intestinal pathobionts promotes their overgrowth during undernutrition," Nature Communications, Nature, vol. 12(1), pages 1-14, December.
    2. Natasa Giallourou & Jason Arnold & Elizabeth T. Rogawski McQuade & Muyiwa Awoniyi & Rose Viguna Thomas Becket & Kenneth Walsh & Jeremy Herzog & Ajay S. Gulati & Ian M. Carroll & Stephanie Montgomery &, 2023. "Giardia hinders growth by disrupting nutrient metabolism independent of inflammatory enteropathy," Nature Communications, Nature, vol. 14(1), pages 1-18, December.

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