SPECIFIC ROLE OF IL-1Β IN URIC ACID-RELATED INFLAMMATION : A NARRATIVE REVIEW

Rona Hawa Kamilah (Biomedical Science Study Program, Faculty of Medicine, Universitas Sriwijaya, South Sumatra, Indonesia)
Salni (Biomedical Department, Faculty of Medicine, Universitas Sriwijaya, South Sumatra, Indonesia)
Ziske Maritska (Biomedical Science Study Program, Faculty of Medicine, Universitas Sriwijaya, South Sumatra, Indonesia)
Fatmawati (Biochemical Deparment, Faculty of Medicine, Universitas Sriwijaya, South Sumatra, Indonesia)

Jurnal Kedokteran dan Kesehatan : Publikasi Ilmiah Fakultas Kedokteran Universitas Sriwijaya
Vol. 11 No. 2 (2024): Jurnal Kedokteran dan Kesehatan : Publikasi Ilmiah Fakultas Kedokteran Univers

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.