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Pancreatic glycoprotein 2 is a first line of defense for mucosal protection in intestinal inflammation

Author

Listed:
  • Yosuke Kurashima

    (The University of Tokyo Distinguished Professor Unit, The Institute of Medical Science, The University of Tokyo
    Chiba University
    The University of Tokyo
    University of California)

  • Takaaki Kigoshi

    (The University of Tokyo Distinguished Professor Unit, The Institute of Medical Science, The University of Tokyo
    Tohoku University)

  • Sayuri Murasaki

    (The University of Tokyo Distinguished Professor Unit, The Institute of Medical Science, The University of Tokyo
    The University of Tokyo)

  • Fujimi Arai

    (The University of Tokyo Distinguished Professor Unit, The Institute of Medical Science, The University of Tokyo
    The University of Tokyo)

  • Kaoru Shimada

    (The University of Tokyo Distinguished Professor Unit, The Institute of Medical Science, The University of Tokyo
    The University of Tokyo)

  • Natsumi Seki

    (Keio University
    Keio University)

  • Yun-Gi Kim

    (Keio University)

  • Koji Hase

    (The University of Tokyo
    Keio University)

  • Hiroshi Ohno

    (RIKEN Center for Integrative Medical Sciences
    Yokohama City University
    Kanagawa Institute of Industrial Science and Technology)

  • Kazuya Kawano

    (RIKEN Center for Integrative Medical Sciences)

  • Hiroshi Ashida

    (Tokyo Medical and Dental University
    Chiba University)

  • Toshihiko Suzuki

    (Tokyo Medical and Dental University)

  • Masako Morimoto

    (Chiba University)

  • Yukari Saito

    (Chiba University)

  • Ai Sasou

    (The University of Tokyo Distinguished Professor Unit, The Institute of Medical Science, The University of Tokyo
    The University of Tokyo)

  • Yuki Goda

    (The University of Tokyo Distinguished Professor Unit, The Institute of Medical Science, The University of Tokyo
    The University of Tokyo)

  • Yoshikazu Yuki

    (The University of Tokyo Distinguished Professor Unit, The Institute of Medical Science, The University of Tokyo
    The University of Tokyo)

  • Yutaka Inagaki

    (Tokai University)

  • Hideki Iijima

    (Osaka University)

  • Wataru Suda

    (RIKEN Center for Integrative Medical Sciences)

  • Masahira Hattori

    (RIKEN Center for Integrative Medical Sciences
    Waseda University)

  • Hiroshi Kiyono

    (The University of Tokyo Distinguished Professor Unit, The Institute of Medical Science, The University of Tokyo
    The University of Tokyo
    University of California
    Chiba University)

Abstract

Increases in adhesive and invasive commensal bacteria, such as Escherichia coli, and subsequent disruption of the epithelial barrier is implicated in the pathogenesis of inflammatory bowel disease (IBD). However, the protective systems against such barrier disruption are not fully understood. Here, we show that secretion of luminal glycoprotein 2 (GP2) from pancreatic acinar cells is induced in a TNF–dependent manner in mice with chemically induced colitis. Fecal GP2 concentration is also increased in Crohn’s diease patients. Furthermore, pancreas-specific GP2-deficient colitis mice have more severe intestinal inflammation and a larger mucosal E. coli population than do intact mice, indicating that digestive-tract GP2 binds commensal E. coli, preventing epithelial attachment and penetration. Thus, the pancreas–intestinal barrier axis and pancreatic GP2 are important as a first line of defense against adhesive and invasive commensal bacteria during intestinal inflammation.

Suggested Citation

  • Yosuke Kurashima & Takaaki Kigoshi & Sayuri Murasaki & Fujimi Arai & Kaoru Shimada & Natsumi Seki & Yun-Gi Kim & Koji Hase & Hiroshi Ohno & Kazuya Kawano & Hiroshi Ashida & Toshihiko Suzuki & Masako M, 2021. "Pancreatic glycoprotein 2 is a first line of defense for mucosal protection in intestinal inflammation," Nature Communications, Nature, vol. 12(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-21277-2
    DOI: 10.1038/s41467-021-21277-2
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    Cited by:

    1. Kensuke Shibata & Chihiro Motozono & Masamichi Nagae & Takashi Shimizu & Eri Ishikawa & Daisuke Motooka & Daisuke Okuzaki & Yoshihiro Izumi & Masatomo Takahashi & Nao Fujimori & James B. Wing & Takahi, 2022. "Symbiotic bacteria-dependent expansion of MR1-reactive T cells causes autoimmunity in the absence of Bcl11b," Nature Communications, Nature, vol. 13(1), pages 1-15, December.

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