Service of Rheumatology, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Avenue Pierre Decker 4, 1011 Lausanne, Switzerland.
Department of Biochemistry, University of Lausanne, 155 Chemin des Boveresses, 1066 Epalinges, Switzerland.
Nat Rev Rheumatol. 2017 Nov;13(11):639-647. doi: 10.1038/nrrheum.2017.155. Epub 2017 Sep 28.
The acute symptoms of gout are triggered by the inflammatory response to monosodium urate crystals, mediated principally by macrophages and neutrophils. Innate immune pathways are of key importance in the pathogenesis of gout, in particular the activation of the NLRP3 inflammasome, which leads to the release of IL-1β and other pro-inflammatory cytokines. The orchestration of this pro-inflammatory cascade involves multiple intracellular and extracellular receptors and enzymes interacting with environmental influences that modulate the inflammatory state. Furthermore, the resolution of inflammation in gout is becoming better understood. This Review highlights recent advances in our understanding of both positive and negative regulatory pathways, as well as the genetic and environmental factors that modulate the inflammatory response. Some of these pathways can be manipulated and present novel therapeutic opportunities for the treatment of acute gout attacks.
痛风的急性症状是由单钠尿酸盐晶体的炎症反应引发的，主要由巨噬细胞和中性粒细胞介导。先天免疫途径在痛风的发病机制中至关重要，特别是 NlRP3 炎性小体的激活，导致白细胞介素-1β和其他促炎细胞因子的释放。这种促炎级联反应的协调涉及多个细胞内和细胞外受体以及与环境影响相互作用的酶，这些影响调节炎症状态。此外，痛风中炎症的消退正在得到更好的理解。这篇综述强调了我们对正负调节途径的理解，以及调节炎症反应的遗传和环境因素的最新进展。其中一些途径可以被操纵，并为治疗急性痛风发作提供新的治疗机会。
