The NLRP3 inflammasome protects against loss of epithelial integrity and mortality during experimental colitis
Open accessAbstract
Decreased expression of the Nlrp3 protein is associated with susceptibility to Crohn's disease. However, the role of Nlrp3 in colitis has not been characterized. Nlrp3 interacts with the adaptor protein ASC to activate caspase-1 in inflammasomes, which are protein complexes responsible for the maturation and secretion of interleukin-1beta (IL-1beta) and IL-18. Here, we showed that mice deficient for Nlrp3 or ASC and caspase-1 were highly susceptible to dextran sodium sulfate (DSS)-induced colitis. Defective inflammasome activation led to loss of epithelial integrity, resulting in systemic dispersion of commensal bacteria, massive leukocyte infiltration, and increased chemokine production in the colon. This process was a consequence of a decrease in IL-18 in mice lacking components of the Nlrp3 inflammasome, resulting in higher mortality rates. Thus, the Nlrp3 inflammasome is critically involved in the maintenance of intestinal homeostasis and protection against colitis.
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The inflammasome can strongly affect gut microbiota composition, as deletion of inflammasome components was associated with loss of epithelial integrity and gut inflammation associated with dysbiosis and bacteremia.
“The inflammasome can indeed strongly affect gut microbiota composition as deletion of inflammasome components was associated with loss of epithelial integrity and gut inflammation associated with dysbiosis and bacteremia [292].”
From Gut-pancreas-liver Axis as a target for treatment of NAFLD/NASH (2020) · cites this paper as [292]
Commensal bacteria and their bioproducts induce inflammasome activation and IL-18 production in the gut, which prevents intestinal barrier disruption and dysbiosis.
“Commensal bacteria and their bioproducts induce inflammasomes activation and IL-18 production in the gut, which, in turn, prevents intestinal barrier disruption and dysbiosis [121,124,131,132,133].”
From Gut Microbiota and Cancer: From Pathogenesis to Therapy (2019) · cites this paper as [133]
Dysbiosis has been observed in mice deficient for inflammasome components including NLRP6, ASC, caspase-1, and IL-18.
“Dysbiosis has been observed in mice deficient for inflammasomes components, including NLRP6, ASC, caspase-1, and IL-18 [131,132,133,134].”
From Gut Microbiota and Cancer: From Pathogenesis to Therapy (2019) · cites this paper as [133]
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- Authors
- Zaki, M. H., Boyd, K. L., Vogel, P., Kastan, M. B., Lamkanfi, M., & Kanneganti, T.-D.
- Affiliations
- St. Jude Children's Research Hospital (US)
- Ghent University (BE)
- Corresponding author
- Kanneganti, Thirumala-Devi
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2010-03
- Volume
- 32
- Issue
- 3
- Pages
- 379-391
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC2982187
- OpenAlex
- W2066327704
- Cited by
- 989
- References
- 57
- Citations by year
- 2026: 36 · 2025: 47 · 2024: 71 · 2023: 56 · 2022: 63 · 2021: 83 · 2020: 50 · 2019: 65 · 2018: 70 · 2017: 57 · 2016: 60 · 2015: 67 · 2014: 68 · 2013: 65 · 2012: 55
- FWCI
- 25.09
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1234 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion)
- Funders
- Yale University
- American Lebanese Syrian Associated Charities (AR056296, CA 21765)
- Vlaamse regering
- National Institutes of Health (CA21765))
- Takeda Oncology
- National Cancer Institute (P30CA021765)
- National Institute of Allergy and Infectious Diseases (R21AI088177)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR056296, AR-056296)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- NLRP3 inflammasome, colitis, DSS-induced colitis, intestinal epithelial integrity, IL-18, caspase-1, ASC, leukocyte infiltration, chemokines, intestinal homeostasis, IL-1β
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Carrier Proteins, Colitis, Cytoskeletal Proteins, Disease Models, Animal, Epithelial Cells, Intestinal Absorption, Mice, Inbred C57BL, Signal Transduction, Dextran Sulfate, Mice, Knockout, Interleukin-18, Cell Proliferation, Apoptosis Regulatory Proteins, Mice, CARD Signaling Adaptor Proteins
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