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

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. Dowling, P. A. Johanesen, T. A. Kufer, J. S. Pedersen, A. Mansell, D. J. Philpott, K. D. Elgass, H. E. Abud, U. Nachbur, B. A. Croker, S. L. Masters and R. L. Ferrero ()
Additional contact information
L. S. Tran: Hudson Institute of Medical Research
L. Ying: Hudson Institute of Medical Research
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
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
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
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
S. L. Masters: WEHI
R. L. Ferrero: Hudson Institute of Medical Research

Nature Communications, 2023, vol. 14, issue 1, 1-18

Abstract: 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.

Date: 2023
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DOI: 10.1038/s41467-023-39487-1

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