Department of Microbiology and Infectious Disease and Immunology Research Group, University of Calgary, 4A18 HRIC, 3330 Hospital Drive NW, Calgary, Alberta T2N 4N1, Canada.
Curr Rheumatol Rep. 2011 Apr;13(2):160-6. doi: 10.1007/s11926-011-0162-1.
Gout is an ancient disease that still plagues us. Its pathogenic culprit, uric acid crystal deposition in tissues, is a strong inflammatory stimulant. In recent years, the mechanisms through which uric acid crystals promote inflammation have been a subject of increasing interest among rheumatologists and immunologists. Uric acid has been identified as an endogenous adjuvant that drives immune responses in the absence of microbial stimulation. Because uric acid is a ubiquitous metabolite that is produced in high quantities upon cellular injury, the ramifications of its effects may be considerable in health and in disease. Uric acid crystals also have been shown to trigger interleukin-1β-mediated inflammation via activation of the NOD-like receptor protein (NLRP)3 inflammasome, a multimolecular complex whose activation appears to be central to many pathological inflammatory conditions. In this article, we review the possible mechanisms of uric acid-mediated inflammation and offer some historical perspectives on what has been learned about the complex effects of a relatively simple substance.
痛风是一种古老的疾病，至今仍困扰着我们。其致病元凶是尿酸盐晶体在组织中的沉积，这是一种强烈的炎症刺激物。近年来，尿酸盐晶体促进炎症的机制一直是风湿病学家和免疫学家关注的热点。尿酸已被确定为一种内源性佐剂，在没有微生物刺激的情况下驱动免疫反应。由于尿酸是一种无处不在的代谢物，在细胞损伤时会大量产生，因此其影响在健康和疾病中可能是相当大的。尿酸盐晶体还被证明可以通过激活 NOD 样受体蛋白（NLRP）3 炎性小体触发白细胞介素 1β 介导的炎症，NLRP3 炎性小体是一种多分子复合物，其激活似乎是许多病理炎症状态的核心。在本文中，我们综述了尿酸介导炎症的可能机制，并从历史角度探讨了相对简单物质的复杂作用。
