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首页> 外文期刊>Nature >Gout-associated uric acid crystals activate the NALP3 inflammasome.
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Gout-associated uric acid crystals activate the NALP3 inflammasome.

机译：痛风相关的尿酸晶体激活了NALP3炎性体。

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摘要

Development of the acute and chronic inflammatory responses known as gout and pseudogout are associated with the deposition of monosodium urate (MSU) or calcium pyrophosphate dihydrate (CPPD) crystals, respectively, in joints and periarticular tissues. Although MSU crystals were first identified as the aetiological agent of gout in the eighteenth century and more recently as a 'danger signal' released from dying cells, little is known about the molecular mechanisms underlying MSU- or CPPD-induced inflammation. Here we show that MSU and CPPD engage the caspase-1-activating NALP3 (also called cryopyrin) inflammasome, resulting in the production of active interleukin (IL)-1beta and IL-18. Macrophages from mice deficient in various components of the inflammasome such as caspase-1, ASC and NALP3 are defective in crystal-induced IL-1beta activation. Moreover, an impaired neutrophil influx is found in an in vivo model of crystal-induced peritonitis in inflammasome-deficient mice or mice deficient in the IL-1beta receptor (IL-1R). These findings provide insight into the molecular processes underlying the inflammatory conditions of gout and pseudogout, and further support a pivotal role of the inflammasome in several autoinflammatory diseases.
机译：被称为痛风和假痛风的急性和慢性炎症反应的发展与分别在关节和关节周围组织中的尿酸钠（MSU）或焦磷酸钙二水合物（CPPD）晶体的沉积有关。尽管MSU晶体在18世纪首次被鉴定为痛风的病因，最近已被确认为垂死细胞释放的“危险信号”，但对MSU或CPPD诱发炎症的分子机制了解甚少。在这里，我们显示MSU和CPPD参与激活caspase-1活化的NALP3（也称为冷冻蛋白）炎性小体，导致产生活性白介素（IL）-1beta和IL-18。缺乏炎性体的各种成分（例如胱天蛋白酶1，ASC和NALP3）的小鼠巨噬细胞在晶体诱导的IL-1β激活中存在缺陷。此外，在炎症小体缺陷型小鼠或IL-1β受体（IL-1R）缺陷型小鼠的晶体诱发的腹膜炎的体内模型中发现中性粒细胞流入受损。这些发现为痛风和假痛风的炎症条件的分子过程提供了见识，并进一步支持了炎性体在几种自身炎症性疾病中的关键作用。

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