Epithelial-microbial crosstalk in polymeric Ig receptor deficient mice

Authors

  • Dag Henrik Reikvam,

    Corresponding author
    1. Department of Pathology and Centre for Immune Regulation, University of Oslo and Oslo University Hospital – Rikshospitalet, Oslo, Norway
    Current affiliation:
    1. Department of Infectious Diseases, Oslo University Hospital – Ulleval, Oslo, Norway
    • Full Correspondence: Prof. Finn-Eirik Johansen, Department of Pathology and Centre for Immune Regulation, Oslo University Hospital – Rikshospitalet, Postboks 4950 Nydalen, N-0424 Oslo, Norway

      Fax: +47-23071511

      e-mail: f.e.johansen@imbv.uio.no

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  • Muriel Derrien,

    1. Laboratory of Microbiology, Wageningen University, Wageningen, The Netherlands
    Current affiliation:
    1. Top Institute Food and Nutrition, Wageningen, The Netherlands
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    • These authors contributed equally to this work.

  • Rejoanoul Islam,

    1. Department of Pathology and Centre for Immune Regulation, University of Oslo and Oslo University Hospital – Rikshospitalet, Oslo, Norway
    2. Laboratory of Microbiology, Wageningen University, Wageningen, The Netherlands
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    • These authors contributed equally to this work.

  • Alexander Erofeev,

    1. Department of Pathology and Centre for Immune Regulation, University of Oslo and Oslo University Hospital – Rikshospitalet, Oslo, Norway
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    • These authors contributed equally to this work.

  • Vedrana Grcic,

    1. Department of Pathology and Centre for Immune Regulation, University of Oslo and Oslo University Hospital – Rikshospitalet, Oslo, Norway
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  • Anders Sandvik,

    1. Department of Pathology and Centre for Immune Regulation, University of Oslo and Oslo University Hospital – Rikshospitalet, Oslo, Norway
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  • Peter Gaustad,

    1. Institute of Microbiology, University of Oslo, Oslo, Norway
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  • Leonardo A. Meza-Zepeda,

    1. Department of Tumor Biology, Oslo University Hospital – The Norwegian Radium Hospital, Oslo, Norway
    2. Norwegian Microarray Consortium,, Department of Molecular Biosciences, University of Oslo, Oslo, Norway
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  • Frode L. Jahnsen,

    1. Department of Pathology and Centre for Immune Regulation, University of Oslo and Oslo University Hospital – Rikshospitalet, Oslo, Norway
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  • Hauke Smidt,

    1. Laboratory of Microbiology, Wageningen University, Wageningen, The Netherlands
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  • Finn-Eirik Johansen

    Corresponding author
    1. Department of Pathology and Centre for Immune Regulation, University of Oslo and Oslo University Hospital – Rikshospitalet, Oslo, Norway
    2. Department of Molecular Biosciences, University of Oslo, Oslo, Norway
    • Full Correspondence: Prof. Finn-Eirik Johansen, Department of Pathology and Centre for Immune Regulation, Oslo University Hospital – Rikshospitalet, Postboks 4950 Nydalen, N-0424 Oslo, Norway

      Fax: +47-23071511

      e-mail: f.e.johansen@imbv.uio.no

    Search for more papers by this author

Abstract

Innate and adaptive mucosal defense mechanisms ensure a homeostatic relationship with the large and complex mutualistic gut microbiota. Dimeric IgA and pentameric IgM are transported across the intestinal epithelium via the epithelial polymeric Ig receptor (pIgR) and provide a significant portion of the first line of natural or adaptive antibody-mediated immune defense of the intestinal mucosa. We found that colonic epithelial cells from pIgR KO mice differentially expressed (more than twofold change) more than 200 genes compared with cells from WT mice, and upregulated the expression of antimicrobial peptides in a commensal-dependent manner. Detailed profiling of microbial communities based on 16S rRNA genes revealed differences in the commensal microbiota between pIgR KO and WT mice. Furthermore, we found that pIgR KO mice showed increased susceptibility to dextran sulfate sodium-induced colitis, and that this was driven by their conventional intestinal microbiota. Thus, in the absence of pIgR, the stability of the commensal microbiota is disturbed, gut homeostasis is compromised, and the outcome of colitis is significantly worsened.

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