痛风性关节炎(gouty arthritis, GA)是一种由大量单钠尿酸盐(monosodium urate, MSU)沉积所导致的急性炎症。MSU晶体引发中性粒细胞胞外诱捕网(neutrophil extracellular traps, NETs)的产生，后者诱发粒细胞和单核细胞释放 促炎细胞因子和趋化因子，使炎症反应进一步加剧。NETs的大量形成会对晶体进行包埋降解，抑制炎症扩散。文章概述了GA的发生、发展及自我缓解过程中中性粒细胞在其中所起到的双重作用，以及参与中性粒细胞NETs形成的相关信号通路。

Gouty arthritis (GA) is an acute inflammatory that is initiated by the precipitation of oversaturated solutions of uric acid as monosodium urate (MSU) crystals, which activates neutrophils to release neutrophil extracellular traps (NETs). NETs further enhance the inflammatory response by inducing neutrophils and monocytes to release pro-inflammatory cytokines and chemokines. However, the increasing number of neutrophils recruited to the sites of MSU deposits allows the formation of aggregated NETs that densely packs MSU crystals and degrades the proinflammatory cytokines, thereby allowing turning down the inflammatory. Here we briefly summarize the dual role of neutrophils during the initiation, development and the resolution of GA, and the signal pathways involved in the regulation of NETs formation.