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The Nlrp6 inflammasome is not required for baseline colonic inner mucus layer formation or function

Journal article
Authors Joana K. Volk
Elisabeth E. L. Nyström
Sjoerd van der Post
Beatriz Martinez Abad
Björn O. Schröder
Åsa Johansson
Frida Svensson
Sofia Jäverfelt
Malin E V Johansson
Gunnar C. Hansson
George M. H. Birchenough
Published in Journal of Experimental Medicine
Volume 216
Issue 11
Pages 2602-2618
ISSN 0022-1007
Publication year 2019
Published at Wallenberg Laboratory
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 2602-2618
Language en
Keywords microbiota, il-18, expression, colitis, protein, cells, interleukin-18, barrier, impact, shape, Immunology, Research & Experimental Medicine
Subject categories Immunology


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.

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