Cited by 832Inflammasome and immune disordersImmune Response and InflammationIL-33, ST2, and ILC Pathways

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Glyburide inhibits the Cryopyrin/Nalp3 inflammasome

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Lamkanfi, Mohamed, Mueller, James L., Vitari, Alberto C., Misaghi, Shahram, Fedorova, Anna, Deshayes, Kurt, Lee, Wyne P., Hoffman, Hal M., Dixit, Vishva M.·2009·Journal of Cell Biology

DOI 10.1083/jcb.200903124PMC PMC2762099

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Abstract

Inflammasomes activate caspase-1 for processing and secretion of the cytokines interleukin-1beta (IL-1beta) and IL-18. Cryopyrin/NALP3/NLRP3 is an essential component of inflammasomes triggered by microbial ligands, danger-associated molecular patterns (DAMPs), and crystals. Inappropriate Cryopyrin activity has been incriminated in the pathogenesis of gouty arthritis, Alzheimer's, and silicosis. Therefore, inhibitors of the Nalp3 inflammasome offer considerable therapeutic promise. In this study, we show that the type 2 diabetes drug glyburide prevented activation of the Cryopyrin inflammasome. Glyburide's cyclohexylurea group, which binds to adenosine triphosphatase (ATP)-sensitive K(+) (K(ATP)) channels for insulin secretion, is dispensable for inflammasome inhibition. Macrophages lacking K(ATP) subunits or ATP-binding cassette transporters also activate the Cryopyrin inflammasome normally. Glyburide analogues inhibit ATP- but not hypothermia-induced IL-1beta secretion from human monocytes expressing familial cold-associated autoinflammatory syndrome-associated Cryopyrin mutations, thus suggesting that inhibition occurs upstream of Cryopyrin. Concurrent with the role of Cryopyrin in endotoxemia, glyburide significantly delays lipopolysaccharide-induced lethality in mice. Therefore, glyburide is the first identified compound to prevent Cryopyrin activation and microbial ligand-, DAMP-, and crystal-induced IL-1beta secretion.

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Authors: Lamkanfi, M., Mueller, J. L., Vitari, A. C., Misaghi, S., Fedorova, A., Deshayes, K., Lee, W. P., Hoffman, H. M., & Dixit, V. M.
Affiliations: Genentech (US)
University of California San Diego (US)
Corresponding author: Dixit, Vishva M.
ORCID: Lamkanfi, Mohamed
Misaghi, Shahram
Lee, Wyne P.
Hoffman, Hal M.
Dixit, Vishva M.
Venue: Journal of Cell Biology
Publisher: Rockefeller University Press
Published: 2009-10-05
Volume: 187
Issue: 1
Pages: 61-70
ISSN: 0021-9525 (ISSN-L)
1540-8140
DOI: 10.1083/jcb.200903124
PMC: PMC2762099
OpenAlex: W2134007048
Cited by: 820
References: 35
Citations by year: 2026: 25 · 2025: 44 · 2024: 63 · 2023: 50 · 2022: 67 · 2021: 52 · 2020: 66 · 2019: 64 · 2018: 62 · 2017: 47 · 2016: 42 · 2015: 68 · 2014: 47 · 2013: 44 · 2012: 31
FWCI: 10.48
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-sa
Locations: The Journal of Cell Biology (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion, cc-by-nc-sa)
PubMed (publishedVersion)
Ghent University Academic Bibliography (Ghent University) (submittedVersion, other-oa)
Funders: National Institute of Allergy and Infectious Diseases (R01AI052430)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
Keywords: glibenclamide, NLRP3 inflammasome, NLRP3, caspase-1, IL-1β, IL-18, ATP-sensitive potassium channels, ABC transporters, monocytes, lipopolysaccharide, endotoxemia, gout, type 2 diabetes drugs, inflammasome inhibitors
MeSH terms: NLR Family, Pyrin Domain-Containing 3 Protein, Adenosine Triphosphatases, Adenosine Triphosphate, Animals, Carrier Proteins, Cells, Cultured, Enzyme Activation, Glyburide, Humans, Hypoglycemic Agents, Inflammation, Lipopolysaccharides, Macrophages, Male, Mice, Inbred BALB C, Mice, Inbred C57BL, Monocytes, Mutation, Random Allocation, Salmonella typhimurium, Mice, Knockout, Caspase 1, Interleukin-18, Mice, Interleukin-1beta

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