First Department of Internal Medicine, Democritus University of Thrace, University General Hospital of Alexandroupolis, Dragana, Alexandroupoli, Greece.
Semin Immunopathol. 2013 Jul;35(4):501-12. doi: 10.1007/s00281-013-0361-0. Epub 2013 Jan 24.
Gout is a prototype crystal-induced inflammatory disorder, characterized by neutrophil infiltration into inflamed joints. The identification of the role of NLRP3 inflammasome in the recognition of monosodium urate crystals and the subsequent release of IL-1β was a milestone in the elucidation of the pathogenesis of this disorder. IL-1β signaling is considered nowadays as the initiatory event that induces gouty inflammation and promotes the recruitment of vast numbers of neutrophils at the sites of inflammation. Crystal-induced neutrophil activation results in apoptosis inhibition, degranulation, superoxide production, cytokine release and, as recently described, formation of neutrophil extracellular traps, further amplifying the inflammatory process. Finally, neutrophil apoptosis and uptake of apoptotic material by macrophages drive the resolution of acute inflammation. In this review, we discuss the recent experimental data regarding the crosstalk between IL-1β and neutrophils in the pathogenesis of acute gout.
痛风是一种典型的晶体诱导炎症性疾病，其特征是中性粒细胞浸润炎症关节。NLRP3 炎性体在识别单钠尿酸盐晶体和随后释放白细胞介素 1β（IL-1β）中的作用的确定是阐明该疾病发病机制的一个里程碑。IL-1β 信号被认为是诱导痛风炎症和促进炎症部位大量中性粒细胞募集的起始事件。晶体诱导的中性粒细胞激活导致细胞凋亡抑制、脱颗粒、超氧化物产生、细胞因子释放，以及最近描述的中性粒细胞细胞外陷阱的形成，进一步放大炎症过程。最后，中性粒细胞凋亡和巨噬细胞摄取凋亡物质驱动急性炎症的消退。在这篇综述中，我们讨论了最近关于 IL-1β 和中性粒细胞在急性痛风发病机制中相互作用的实验数据。
