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

Abstract

The specific role of IL-1β in uric acid-related inflammation: A Review. 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.