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.

中文翻译：

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痛风炎症：机制和治疗目标

痛风的急性症状主要由巨噬细胞和嗜中性粒细胞介导，对尿酸单钠晶体的炎症反应引起。先天性免疫途径在痛风的发病机理中至关重要，特别是NLRP3炎性小体的激活，从而导致IL-1β和其他促炎性细胞因子的释放。这种促炎性级联的编排涉及多个细胞内和细胞外受体和酶，这些酶与调节炎症状态的环境影响相互作用。此外，人们对痛风炎症的解决也越来越了解。这篇综述强调了我们对正调控途径和负调控途径以及调节炎症反应的遗传和环境因素的最新进展。