Cited by 785Inflammasome and immune disordersFatty Acid Research and HealthImmune Response and Inflammation

Omega-3 fatty acids prevent inflammation and metabolic disorder through inhibition of NLRP3 inflammasome activation

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Yan, Yiqing, Jiang, Wei, Spinetti, Thibaud, Tardivel, Aubry, Castillo, Rosa, Bourquin, Carole, Guarda, Greta, Tian, Zhigang +2 more·2013·Immunity

Abstract

Omega-3 fatty acids (ω-3 FAs) have potential anti-inflammatory activity in a variety of inflammatory human diseases, but the mechanisms remain poorly understood. Here we show that stimulation of macrophages with ω-3 FAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and other family members, abolished NLRP3 inflammasome activation and inhibited subsequent caspase-1 activation and IL-1β secretion. In addition, G protein-coupled receptor 120 (GPR120) and GPR40 and their downstream scaffold protein β-arrestin-2 were shown to be involved in inflammasome inhibition induced by ω-3 FAs. Importantly, ω-3 FAs also prevented NLRP3 inflammasome-dependent inflammation and metabolic disorder in a high-fat-diet-induced type 2 diabetes model. Our results reveal a mechanism through which ω-3 FAs repress inflammation and prevent inflammation-driven diseases and suggest the potential clinical use of ω-3 FAs in gout, autoinflammatory syndromes, or other NLRP3 inflammasome-driven inflammatory diseases.

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Crossref · 10.1016/j.immuni.2013.05.015

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  • The anti-inflammatory effects of omega-3 fatty acids seem to be mediated by binding to the G-protein-coupled receptor 120 and inhibition of NLRP3 inflammasome activity.

    “The anti-inflammatory effects of omega-3 fatty acids seems to be mediated by binding to the G-protein–coupled receptor 120 and inhibition of NLRP3 inflammasome activity (53,54).”

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Authors
Yan, Y., Jiang, W., Spinetti, T., Tardivel, A., Castillo, R., Bourquin, C., Guarda, G., Tian, Z., Tschopp, J., & Zhou, R.
Affiliations
  • University of Science and Technology of China (CN)
  • University of Fribourg (CH)
  • University of Lausanne (CH)
Corresponding author
  • Tian, Zhigang
  • Zhou, Rongbin
Venue
Immunity
Publisher
Elsevier BV
Published
2013-06
Volume
38
Issue
6
Pages
1154-1163
ISSN
1074-7613 (ISSN-L)
OpenAlex
W1998522372
Cited by
784
References
48
Citations by year
2026: 53 · 2025: 65 · 2024: 55 · 2023: 68 · 2022: 51 · 2021: 77 · 2020: 51 · 2019: 63 · 2018: 70 · 2017: 63 · 2016: 57 · 2015: 57 · 2014: 36 · 2013: 17
FWCI
24.95
Type
journal article
Language
en
Open access
Locations
  • Immunity (publishedVersion)
  • PubMed (publishedVersion)
  • IRIS (submittedVersion)
  • SERVAL (Université de Lausanne) (submittedVersion)
  • Open Access CRIS of the University of Bern
Funders
  • National Natural Science Foundation of China (81222040, 31200659, 81273318, 91029303)
  • Ministry of Education of the People's Republic of China (20123402110010, 20123402120001)
  • University of Science and Technology of China
  • Chinese Academy of Sciences
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
  • Louis-Jeantet Foundation
  • Fundamental Research Funds for the Central Universities
  • Program for New Century Excellent Talents in University
  • Seventh Framework Programme
  • National Key Research and Development Program of China (2013CB944904)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
omega-3 fatty acids, NLRP3 inflammasome, caspase-1 activation, IL-1β secretion, macrophages, GPR120, GPR40, β-arrestin2, eicosapentaenoic acid, docosahexaenoic acid, type 2 diabetes, metabolic disorders, inflammation, gout, autoinflammatory disease, high-fat diet
MeSH terms
NLR Family, Pyrin Domain-Containing 3 Protein, beta-Arrestins, beta-Arrestin 2, Animals, Carrier Proteins, Cells, Cultured, Diabetes Mellitus, Type 2, Docosahexaenoic Acids, Enzyme Activation, Inflammation, Macrophages, Mice, Inbred C57BL, Eicosapentaenoic Acid, Fatty Acids, Omega-3, Mice, Knockout, Arrestins, Caspase 1, Receptors, G-Protein-Coupled, Mice, Interleukin-1beta, Inflammasomes, Diet, High-Fat

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