Ziske Maritska
Biomedical Science Study Program, Faculty of Medicine, Universitas Sriwijaya, South Sumatra, Indonesia

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SPECIFIC ROLE OF IL-1Β IN URIC ACID-RELATED INFLAMMATION : A NARRATIVE REVIEW Rona Hawa Kamilah; Salni; Ziske Maritska; Fatmawati
Jurnal Kedokteran dan Kesehatan : Publikasi Ilmiah Fakultas Kedokteran Universitas Sriwijaya Vol. 11 No. 2 (2024): Jurnal Kedokteran dan Kesehatan : Publikasi Ilmiah Fakultas Kedokteran Univers
Publisher : Fakultas Kedokteran Universitas Sriwijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.32539/jkk.v11i2.396

Abstract

Inflammatory conditions in hyperuricemia are caused by monosodium urate crystals that induce the release of IL-1β, marking a crucial milestone in the pathogenesis of hyperuricemia. Several studies have linked the relationship between serum uric acid levels and the release of IL-1β. IL-1β plays a key role in the pathogenesis of gout. The IL-1β signaling is currently considered an initiating event that triggers uric acid inflammation and promotes the recruitment of a large number of neutrophils to the inflammatory site. Neutrophil activation caused by crystals results in the inhibition of apoptosis, degranulation, the release of reactive oxygen species (ROS), TNF-α, IL-1β, and PGE2, as well as the formation of extracellular neutrophil tissue, further reinforcing the inflammatory process. Recent research indicates that hyperuricemia patients have significantly higher levels of IL-1β. Other studies suggest that elevated IL-1β levels correlate with a more severe anatomical pathology in the joint tissues of rat ankles, including synovial hyperplasia, cartilage damage, and bone erosion.