Journal
CELL
Volume 156, Issue 5, Pages 1045-1059Publisher
CELL PRESS
DOI: 10.1016/j.cell.2014.01.026
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Funding
- Weizmann Institute
- Department of Veterinary Resources
- Canadian Institutes of Health Research (CIHR)
- Charles Best Canada graduate scholarship
- Boehringer Ingelheim Fonds PhD Fellowship
- Friends of Tel Aviv Sourasky Medical Center Foundation
- Yael and Rami Ungar, Israel
- Abisch Frenkel Foundation for the Promotion of Life Sciences
- Gurwin Family Fund for Scientific Research
- Leona M. and Harry B. Helmsley Charitable Trust
- Crown Endowment Fund for Immunological Research
- Estate of Jack Gitlitz
- Estate of Lydia Hershkovich
- European Research Council
- Kenneth Rainin Foundation
- German-Israel Binational Foundation
- Israel Science Foundation
- Minerva Foundation
- Alon Foundation
- CIHR
- US Department of Defense
- Blavatnik Family Foundation
- MRC [MR/J006874/1] Funding Source: UKRI
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Mucusproduction by goblet cells of the large intestine serves as a crucial antimicrobial protective mechanism at the interface between the eukaryotic and prokaryotic cells of the mammalian intestinal ecosystem. However, the regulatory pathways involved in goblet cell-induced mucus secretion remain largely unknown. Here, we demonstrate that the NLRP6 inflammasome, a recently described regulator of colonic microbiota composition and biogeographical distribution, is a critical orchestrator of goblet cell mucin granule exocytosis. NLRP6 deficiency leads to defective autophagy in goblet cells and abrogated mucus secretion into the large intestinal lumen. Consequently, NLRP6 inflammasome-deficient mice are unable to clear enteric pathogens from the mucosal surface, rendering them highly susceptible to persistent infection. This study identifies an innate immune regulatory pathway governing goblet cell mucus secretion, linking nonhematopoietic inflammasome signaling to autophagy and highlighting the goblet cell as a critical innate immune player in the control of intestinal host-microbial mutualism.
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