Cited by 238Inflammasome and immune disordersImmune Response and InflammationCancer, Lipids, and Metabolism

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UCP2-induced fatty acid synthase promotes NLRP3 inflammasome activation during sepsis

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Moon, Jong-Seok, Lee, Seonmin, Park, Mi-Ae, Siempos, Ilias I., Haslip, Maria, Lee, Patty J., Yun, Mijin, Kim, Chun K., Howrylak, Judie, Ryter, Stefan W., Nakahira, Kiichi, Choi, Augustine M.K.·2015·Journal of Clinical Investigation

DOI 10.1172/jci78253PMC PMC4319445

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Abstract

Cellular lipid metabolism has been linked to immune responses; however, the precise mechanisms by which de novo fatty acid synthesis can regulate inflammatory responses remain unclear. The NLRP3 inflammasome serves as a platform for caspase-1-dependent maturation and secretion of proinflammatory cytokines. Here, we demonstrated that the mitochondrial uncoupling protein-2 (UCP2) regulates NLRP3-mediated caspase-1 activation through the stimulation of lipid synthesis in macrophages. UCP2-deficient mice displayed improved survival in a mouse model of polymicrobial sepsis. Moreover, UCP2 expression was increased in human sepsis. Consistently, UCP2-deficient mice displayed impaired lipid synthesis and decreased production of IL-1β and IL-18 in response to LPS challenge. In macrophages, UCP2 deficiency suppressed NLRP3-mediated caspase-1 activation and NLRP3 expression associated with inhibition of lipid synthesis. In UCP2-deficient macrophages, inhibition of lipid synthesis resulted from the downregulation of fatty acid synthase (FASN), a key regulator of fatty acid synthesis. FASN inhibition by shRNA and treatment with the chemical inhibitors C75 and cerulenin suppressed NLRP3-mediated caspase-1 activation and inhibited NLRP3 and pro-IL-1β gene expression in macrophages. In conclusion, our results suggest that UCP2 regulates the NLRP3 inflammasome by inducing the lipid synthesis pathway in macrophages. These results identify UCP2 as a potential therapeutic target in inflammatory diseases such as sepsis.

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Authors: Moon, J.-S., Lee, S., Park, M.-A., Siempos, I. I., Haslip, M., Lee, P. J., Yun, M., Kim, C. K., Howrylak, J., Ryter, S. W., Nakahira, K., & Choi, A. M. K.
Affiliations: NewYork–Presbyterian Hospital (US)
Brigham and Women's Hospital (US)
Yale University (US)
Pennsylvania State University (US)
ORCID: Lee, Seonmin
Park, Mi-Ae
Lee, Patty J.
Yun, Mijin
Kim, Chun K.
Howrylak, Judie
Ryter, Stefan W.
Nakahira, Kiichi
Choi, Augustine M.K.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2015-01-09
Volume: 125
Issue: 2
Pages: 665-680
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci78253
PMC: PMC4319445
OpenAlex: W2064173000
Cited by: 238
References: 70
Citations by year: 2026: 1 · 2025: 7 · 2024: 16 · 2023: 23 · 2022: 26 · 2021: 33 · 2020: 32 · 2019: 24 · 2018: 24 · 2017: 28 · 2016: 15 · 2015: 9
FWCI: 11.01
Type: journal article
Language: en
Status: Retracted
Update notices: retraction (2023-03-15)
Open access: green
www.ncbi.nlm.nih.gov
Locations: Journal of Clinical Investigation (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
YUHSpace (Yonsei University Medical Library) (submittedVersion, cc-by-nc-nd)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: Strong
European Society of Intensive Care Medicine
National Institutes of Health
College of Veterinary Medicine, Cornell University
Weill Cornell Medical College
National Heart, Lung, and Blood Institute (R01HL055330, R01HL079904, P01HL108801, R01HL060234, R01HL112747, P01HL114501)
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 › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
Keywords: UCP2, fatty acid synthase, NLRP3 inflammasome, sepsis, macrophages, lipid metabolism, caspase-1 activation, IL-1β, IL-18, lipopolysaccharide, mitochondrial uncoupling, cerulenin, C75, therapeutic target
MeSH terms: NLR Family, Pyrin Domain-Containing 3 Protein, Uncoupling Protein 2, Animals, Carrier Proteins, Enzyme Induction, Humans, Ion Channels, Lipids, Macrophages, Down-Regulation, Mice, Knockout, Sepsis, Caspase 1, Interleukin-18, Mitochondrial Proteins, Mice, Interleukin-1beta, Fatty Acid Synthase, Type I, Inflammasomes

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UCP2-induced fatty acid synthase promotes NLRP3 inflammasome activation during sepsis

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