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The Nlrp6 inflammasome is not required for baseline colonic inner mucus layer formation or function
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2019 (English)In: Journal of Experimental Medicine, ISSN 0022-1007, E-ISSN 1540-9538, Vol. 216, no 11, p. 2602-2618Article in journal (Refereed) Published
Abstract [en]

The inner mucus layer (IML) is a critical barrier that protects the colonic epithelium from luminal threats and inflammatory bowel disease. Innate immune signaling is thought to regulate IML formation via goblet cell Nlrp6 inflammasome activity that controls secretion of the mucus structural component Muc2. We report that isolated colonic goblet cells express components of several inflammasomes; however, analysis of IML properties in multiple inflammasome-deficient mice, including littermate-controlled Nlrp6−/−, detect a functional IML barrier in all strains. Analysis of mice lacking inflammasome substrate cytokines identifies a defective IML in Il18−/− mice, but this phenotype is ultimately traced to a microbiota-driven, Il18-independent effect. Analysis of phenotypic transfer between IML-deficient and IML-intact mice finds that the Bacteroidales family S24-7 (Muribaculaceae) and genus Adlercrutzia consistently positively covary with IML barrier function. Together, our results demonstrate that baseline IML formation and function is independent of inflammasome activity and highlights the role of the microbiota in determining IML barrier function.

Place, publisher, year, edition, pages
Rockefeller University Press, 2019. Vol. 216, no 11, p. 2602-2618
National Category
Gastroenterology and Hepatology Immunology Microbiology
Identifiers
URN: urn:nbn:se:umu:diva-166014DOI: 10.1084/jem.20190679ISI: 000495355800013PubMedID: 31420376OAI: oai:DiVA.org:umu-166014DiVA, id: diva2:1376357
Funder
Swedish Research Council, 2015-00656Swedish Cancer SocietyKnut and Alice Wallenberg FoundationTorsten Söderbergs stiftelseNIH (National Institute of Health), U01AI095473Swedish Foundation for Strategic Research Available from: 2019-12-09 Created: 2019-12-09 Last updated: 2019-12-11Bibliographically approved

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