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NOD1 mediates interleukin-18 processing in epithelial cells responding to Helicobacter pylori infection in mice

Author

Listed:
  • L. S. Tran

    (Hudson Institute of Medical Research
    Monash University)

  • L. Ying

    (Hudson Institute of Medical Research
    Monash University)

  • K. D’Costa

    (Hudson Institute of Medical Research)

  • G. Wray-McCann

    (Hudson Institute of Medical Research)

  • G. Kerr

    (Monash University)

  • L. Le

    (Hudson Institute of Medical Research
    Monash University)

  • C. C. Allison

    (Hudson Institute of Medical Research)

  • J. Ferrand

    (Hudson Institute of Medical Research)

  • H. Chaudhry

    (Hudson Institute of Medical Research)

  • J. Emery

    (Hudson Institute of Medical Research
    Monash University)

  • A. De Paoli

    (Hudson Institute of Medical Research)

  • N. Colon

    (Hudson Institute of Medical Research)

  • S. Creed

    (Monash University)

  • M. Kaparakis-Liaskos

    (Hudson Institute of Medical Research)

  • J. Como

    (Hudson Institute of Medical Research)

  • J. K. Dowling

    (Hudson Institute of Medical Research)

  • P. A. Johanesen

    (Monash University)

  • T. A. Kufer

    (Institute of Nutritional Medicine)

  • J. S. Pedersen

    (TissuPath)

  • A. Mansell

    (Hudson Institute of Medical Research
    Monash University)

  • D. J. Philpott

    (University of Toronto)

  • K. D. Elgass

    (Monash University)

  • H. E. Abud

    (Monash University)

  • U. Nachbur

    (WEHI)

  • B. A. Croker

    (Harvard Medical School
    WEHI)

  • S. L. Masters

    (WEHI)

  • R. L. Ferrero

    (Hudson Institute of Medical Research
    Monash University
    WEHI)

Abstract

The interleukin-1 family members, IL-1β and IL-18, are processed into their biologically active forms by multi-protein complexes, known as inflammasomes. Although the inflammasome pathways that mediate IL-1β processing in myeloid cells have been defined, those involved in IL-18 processing, particularly in non-myeloid cells, are still not well understood. Here we report that the host defence molecule NOD1 regulates IL-18 processing in mouse epithelial cells in response to the mucosal pathogen, Helicobacter pylori. Specifically, NOD1 in epithelial cells mediates IL-18 processing and maturation via interactions with caspase-1, instead of the canonical inflammasome pathway involving RIPK2, NF-κB, NLRP3 and ASC. NOD1 activation and IL-18 then help maintain epithelial homoeostasis to mediate protection against pre-neoplastic changes induced by gastric H. pylori infection in vivo. Our findings thus demonstrate a function for NOD1 in epithelial cell production of bioactive IL-18 and protection against H. pylori-induced pathology.

Suggested Citation

  • L. S. Tran & L. Ying & K. D’Costa & G. Wray-McCann & G. Kerr & L. Le & C. C. Allison & J. Ferrand & H. Chaudhry & J. Emery & A. De Paoli & N. Colon & S. Creed & M. Kaparakis-Liaskos & J. Como & J. K. , 2023. "NOD1 mediates interleukin-18 processing in epithelial cells responding to Helicobacter pylori infection in mice," Nature Communications, Nature, vol. 14(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-39487-1
    DOI: 10.1038/s41467-023-39487-1
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    References listed on IDEAS

    as
    1. Paras K. Anand & R. K. Subbarao Malireddi & John R. Lukens & Peter Vogel & John Bertin & Mohamed Lamkanfi & Thirumala-Devi Kanneganti, 2012. "NLRP6 negatively regulates innate immunity and host defence against bacterial pathogens," Nature, Nature, vol. 488(7411), pages 389-393, August.
    2. Ueli Nachbur & Che A. Stafford & Aleksandra Bankovacki & Yifan Zhan & Lisa M. Lindqvist & Berthe K. Fiil & Yelena Khakham & Hyun-Ja Ko & Jarrod J. Sandow & Hendrik Falk & Jessica K. Holien & Diep Chau, 2015. "A RIPK2 inhibitor delays NOD signalling events yet prevents inflammatory cytokine production," Nature Communications, Nature, vol. 6(1), pages 1-13, May.
    Full references (including those not matched with items on IDEAS)

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