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Omega-3 Free Fatty Acids Suppress Macrophage Inflammasome Activation by Inhibiting NF-κB Activation and Enhancing Autophagy
Open accessAbstract
The omega-3 (ω3) fatty acid docosahexaenoic acid (DHA) can suppress inflammation, specifically IL-1β production through poorly understood molecular mechanisms. Here, we show that DHA reduces macrophage IL-1β production by limiting inflammasome activation. Exposure to DHA reduced IL-1β production by ligands that stimulate the NLRP3, AIM2, and NAIP5/NLRC4 inflammasomes. The inhibition required Free Fatty Acid Receptor (FFAR) 4 (also known as GPR120), a G-protein coupled receptor (GPR) known to bind DHA. The exposure of cells to DHA recruited the adapter protein β-arrestin1/2 to FFAR4, but not to a related lipid receptor. DHA treatment reduced the initial inflammasome priming step by suppressing the nuclear translocation of NF-κB. DHA also reduced IL-1β levels by enhancing autophagy in the cells. As a consequence macrophages derived from mice lacking the essential autophagy protein ATG7 were partially resistant to suppressive effects of DHA. Thus, DHA suppresses inflammasome activation by two distinct mechanisms, inhibiting the initial priming step and by augmenting autophagy, which limits inflammasome activity.
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“n-3 PUFAs, in addition to modulating eicosanoid synthesis, can also inhibit the activation of NFκB in skeletal muscle cells and other cell types in vitro (see Section 2.3) [69,70,71,72].”
From Potential Roles of n-3 PUFAs during Skeletal Muscle Growth and Regeneration (2018) · cites this paper as [71]
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Schroder, K., & Tschopp, J. (2010) · Cell · doi:10.1016/j.cell.2010.01.040 · Cited by 5,475
Bauernfeind, F. G., Horvath, G. L., Stutz, A., Alnemri, E. S., MacDonald, K. L., Speert, D. P., Fernandes‐Alnemri, T., Wu, J., Monks, B. G., Fitzgerald, K. A., et al. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0901363 · Cited by 3,087
Oh, D. Y., Talukdar, S., Bae, E. J., Imamura, T., Morinaga, H., Fan, W., Li, P., Lu, W. J., Watkins, S. M., & Olefsky, J. M. (2010) · Cell · doi:10.1016/j.cell.2010.07.041 · Cited by 2,428
Fatty acid–induced NLRP3-ASC inflammasome activation interferes with insulin signaling
Wen, H., Gris, D., Lei, Y., Jha, S., Zhang, L., Huang, M. T.-H., Brickey, W. J., & Ting, J. P.-Y. (2011) · Nature Immunology · doi:10.1038/ni.2022 · Cited by 1,698
Shi, C.-S., Shenderov, K., Huang, N.-N., Kabat, J., Abu-Asab, M., Fitzgerald, K. A., Sher, A., & Kehrl, J. H. (2012) · Nature Immunology · doi:10.1038/ni.2215 · Cited by 1,367
Self-citationThe role of β-arrestins in the termination and transduction of G-protein-coupled receptor signals
Luttrell, L. M., & Lefkowitz, R. J. (2002) · Journal of Cell Science · doi:10.1242/jcs.115.3.455 · Cited by 1,123
Yan, Y., Jiang, W., Spinetti, T., Tardivel, A., Castillo, R., Bourquin, C., Guarda, G., Tian, Z., Tschopp, J., & Zhou, R. (2013) · Immunity · doi:10.1016/j.immuni.2013.05.015 · Cited by 784
Csak, T., Ganz, M., Pespisa, J., Kodys, K., Dolganiuc, A., & Szabo, G. (2011) · Hepatology · doi:10.1002/hep.24341 · Cited by 645
Mortensen, M., Ferguson, D. J. P., Edelmann, M. J., Kessler, B. M., Morten, K., Komatsu, M., & Simon, A. K. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0913170107 · Cited by 400
Kiecolt-Glaser, J. K., Belury, M. A., Andridge, R., Malarkey, W. B., Hwang, B. S., & Glaser, R. (2012) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2012.05.011 · Cited by 233
Jing, K., Song, K., Shin, S., Kim, N., Jeong, S., Oh, H.-R., Park, J.-H., Seo, K.-S., Heo, J. Y., Han, J., et al. (2011) · Autophagy · doi:10.4161/auto.7.11.16658 · Cited by 208
Shin, S., Jing, K., Jeong, S., Kim, N., Song, K., Heo, J. Y., Park, J.-H., Seo, K.-S., Han, J., Park, J., et al. (2013) · BioMed Research International · doi:10.1155/2013/568671 · Cited by 163
Biswas, D., Qureshi, O. S., Lee, W.-Y. J., Croudace, J. E., Mura, M., & Lammas, D. A. (2008) · BMC Immunology · doi:10.1186/1471-2172-9-35 · Cited by 161
Chapter 2 Methods for Monitoring Autophagy Using GFP‐LC3 Transgenic Mice
Mizushima, N. (2009) · Methods in enzymology on CD-ROM/Methods in enzymology · doi:10.1016/s0076-6879(08)03602-1 · Cited by 161
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Hara, T., Hirasawa, A., Ichimura, A., Kimura, I., & Tsujimoto, G. (2011) · Journal of Pharmaceutical Sciences · doi:10.1002/jps.22639 · Cited by 159
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Decuypere, J.-P., Kindt, D., Luyten, T., Welkenhuyzen, K., Missiaen, L., SMEDT, H. D., Bultynck, G., & Parys, J. B. (2013) · PLoS ONE · doi:10.1371/journal.pone.0061020 · Cited by 113
Inflammasome Activation of IL‐1 Family Mediators in Response to Cutaneous Photodamage†
Nasti, T. H., & Timares, L. (2012) · Photochemistry and Photobiology · doi:10.1111/j.1751-1097.2012.01182.x · Cited by 107
Free Fatty Acids-Sensing G Protein-Coupled Receptors in Drug Targeting and Therapeutics
Yonezawa, T., Kurata, R., Yoshida, K., Murayama, M. A., Cui, X., & Hasegawa, A. (2013) · Current Medicinal Chemistry · doi:10.2174/09298673113209990168 · Cited by 104
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Metadata
- Authors
- Williams-Bey, Y., Boularan, C., Vural, A., Huang, N.-N., Hwang, I.-Y., Shan-Shi, C., & Kehrl, J. H.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Kehrl, John H.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2014-06-09
- Volume
- 9
- Issue
- 6
- Pages
- e97957
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC4049592
- OpenAlex
- W2062456565
- Cited by
- 215
- References
- 18
- Citations by year
- 2026: 15 · 2025: 12 · 2024: 10 · 2023: 11 · 2022: 19 · 2021: 28 · 2020: 23 · 2019: 13 · 2018: 19 · 2017: 19 · 2016: 21 · 2015: 23 · 2014: 2
- FWCI
- 8.88
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases
- 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
- docosahexaenoic acid, omega-3 fatty acids, macrophages, inflammasome activation, IL-1β production, NLRP3 inflammasome, AIM2 inflammasome, free fatty acid receptor 4, GPR120, NF-κB nuclear translocation, autophagy, ATG7
- MeSH terms
- beta-Arrestins, Animals, Autophagy, Bone Marrow Cells, Calcium, Cell Nucleus, Docosahexaenoic Acids, Gene Expression Regulation, HeLa Cells, Humans, Lipopolysaccharides, Macrophage Activation, Macrophages, Mice, Inbred C57BL, NF-kappa B, Arrestins, Active Transport, Cell Nucleus, Intracellular Space, Receptors, G-Protein-Coupled, Mice, Interleukin-1beta, Inflammasomes
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