| 中文摘要 |
期刊連結：http://www.gouthyperuricemia.comPurpose Gout is characterized by recurrent attacks of acute inflammation that causes sudden and severe pain, swelling and tenderness mostly affecting the joints of fingers and feet. In the inflammatory course of gouty arthritis, monocytes activate the NALP3 inflammasome (NLRP3) in response to monosodium urate (MSU) crystals. This results in the secretion of the pro-inflammatory interleukin (IL)-1β. This review provides an understanding of how MSU crystals lead to the spontaneous activation of NLRP3. Surprisingly, inflammatory symptoms in gout attenuate within a few days despite the ongoing presence of MSU crystals in the affected tissue. A recent manuscript explains this formerly enigmatic process of self-limiting inflammation. Findings After the uptake of MSU crystals, intracellular events in monocytes cause a massive drop in the intracellular potassium concentration. This spontaneously activates the NALP3 inflammasome. Thereby produced and secreted IL-1β attracts neutrophils to support the local immune response. Recruited neutrophils promote the enigmatic process of self-limiting in gout as follows: in the presence of MSU crystals, neutrophil granulocytes, the first cells to arrive at the site of inflammation, eject their DNA decorated with antimicrobial proteins to create neutrophil extracellular traps (NETs). These NETs aggregate and effectively immobilize and degrade cytokines and chemokines, supporting the resolution of inflammation. Conclusion In summary, monocytes and neutrophils play crucial roles for the induction and resolution of MSU crystal-induced inflammation. |
