CD39 inhibits increased inflammation and promotes resolution of gout

Abstract Background Gout is a self-limiting inflammatory arthritis induced by the formation of urate crystals due to hyperuricemia. Recent studies have shown that the pathogenesis of gout involves the participation of extracellular ATP, and the synergistic effect of MSU and extracellular ATP can cause gout. CD39 is an ATP hydrolase that is distributed on the surface of macrophages and almost all other immune cells, and it can inhibit inflammation caused by ATP. This suggests that CD39 may inhibit the aggravation of gout inflammation and participate in the remission mechanism of gout. Methods The expression of CD39 mRNA in PBMCs from gout patients, PBMCS from gout model rats and THP-1 cells stimulated by MSU were detected and analyzed. CD39 knockdown was carried out by lentivirus in a monosodium urate (MSU) induced rat model, and CD39 inhibitor was used in MSU induced mouse model. After CD39 was blocked, the activation level of NLRP3 inflammasome and the incidence of gout were observed. Results The results showed that the deletion of CD39 aggravated MSU-induced gouty arthritis and delayed the remission of gout. Furthermore, it promoted the activation of the NLRP3 inflammasome signaling pathway and the release of IL-1βin macrophages. Conclusions Our results confirm that CD39 is elevated in the gout inflammatory environment, and its presence inhibits the aggravation of inflammation and promotes the resolution of gout.