痛风炎症机制。
Mechanisms of inflammation in gout.
机构信息
Service de Rheumatologie, Centre Hospitalier Universitaire Vaudois, Université de Lausanne, Avenue Pierre Decker, 1011 Lausanne, Suisse.
出版信息
Arthritis Res Ther. 2010;12(2):206. doi: 10.1186/ar2952. Epub 2010 Apr 26.
An acute attack of gout is a paradigm of acute sterile inflammation, as opposed to pyogenic inflammation. Recent studies suggest that the triggering of IL-1beta release from leucocytes lies at the heart of a cascade of processes that involves multiple cytokines and mediators. The NLRP3 inflammasome appears to have a specific role in this regard, but the biochemical events leading to its activation are still not well understood. We review the known mechanisms that underlie the inflammatory process triggered by urate crystals and suggest areas that require further research.
痛风急性发作是急性无菌性炎症的典范,与化脓性炎症相反。最近的研究表明,白细胞中白细胞介素-1β的释放触发了一系列涉及多种细胞因子和介质的过程。NLRP3 炎性小体在这方面似乎具有特定的作用,但其激活的生化事件仍未得到很好的理解。我们回顾了尿酸盐晶体引发炎症过程的已知机制,并提出了需要进一步研究的领域。