Cited by 338Gout, Hyperuricemia, Uric AcidImmune Response and InflammationInflammasome and immune disorders

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Uric acid promotes an acute inflammatory response to sterile cell death in mice

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Kono, Hajime, Chen, Chun-Jen, Ontiveros, Fernando, Rock, Kenneth L.·2010·Journal of Clinical Investigation

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Abstract

Necrosis stimulates inflammation, and this response is medically relevant because it contributes to the pathogenesis of a number of diseases. It is thought that necrosis stimulates inflammation because dying cells release proinflammatory molecules that are recognized by the immune system. However, relatively little is known about the molecular identity of these molecules and their contribution to responses in vivo. Here, we investigated the role of uric acid in the inflammatory response to necrotic cells in mice. We found that dead cells not only released intracellular stores of uric acid but also produced it in large amounts postmortem as nucleic acids were degraded. Using newly developed Tg mice that have reduced levels of uric acid either intracellularly and/or extracellularly, we found that uric acid depletion substantially reduces the cell death-induced inflammatory response. Similar results were obtained with pharmacological treatments that reduced uric acid levels either by blocking its synthesis or hydrolyzing it in the extracellular fluids. Importantly, uric acid depletion selectively inhibited the inflammatory response to dying cells but not to microbial molecules or sterile irritant particles. Collectively, our data identify uric acid as a proinflammatory molecule released from dying cells that contributes significantly to the cell death-induced inflammatory responses in vivo.

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Authors: Kono, H., Chen, C.-J., Ontiveros, F., & Rock, K. L.
Affiliations: University of Massachusetts Chan Medical School (US)
National Taiwan University (TW)
Corresponding author: Rock, Kenneth L.
ORCID: Kono, Hajime
Chen, Chun-Jen
Rock, Kenneth L.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2010-06-01
Volume: 120
Issue: 6
Pages: 1939-1949
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci40124
PMC: PMC2877935
OpenAlex: W2092946161
Cited by: 337
References: 34
Citations by year: 2026: 7 · 2025: 16 · 2024: 16 · 2023: 13 · 2022: 19 · 2021: 18 · 2020: 24 · 2019: 17 · 2018: 27 · 2017: 24 · 2016: 33 · 2015: 22 · 2014: 26 · 2013: 22 · 2012: 29
FWCI: 18.71
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
eScholarship@UMassChan (submittedVersion)
Institutional Repositories DataBase (IRDB) (submittedVersion)
Funders: Sanofi
American Asthma Foundation
National Institutes of Health (DK32520)
National Institute of Allergy and Infectious Diseases (R01AI043543, R01AI078287)
National Institute of Diabetes and Digestive and Kidney Diseases (DK 32520, P30DK032520)
Topics: Health Sciences › Medicine › Nephrology › Gout, Hyperuricemia, Uric Acid
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords: uric acid, sterile inflammation, necrosis, cell death, inflammation, nucleic acid degradation, proinflammatory molecules, innate immunity
MeSH terms: Animals, Cells, Immune System, Inflammation, Mice, Inbred C57BL, Mice, Inbred Strains, Mice, Transgenic, Necrosis, Uric Acid, Cell Death, Mice

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Uric acid promotes an acute inflammatory response to sterile cell death in mice

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