Rationale: The role of Monosodium Urate (MSU) crystals in gout pathophysiology is well described, as is the major impact of IL-1β in the inflammatory reaction that constitutes the hallmark of the disease. However, despite the discovery of the NLRP3 inflammasome and its role as a Pattern Recognition Receptor linking the detection of a danger signal (MSU) to IL-1β secretion in vitro, the precise mechanisms leading to joint inflammation in gout patients are still poorly understood.

Methods: Acute urate crystal inflammation was obtained by subcutaneous injections of MSU crystals in mice. Symptoms were followed by scoring, cytokine quantification by ELISA and western blot, gene expression by RT-qPCR and RNAseq; Magnetic Resonance Imaging was also used to assess inflammation.

Results: We provide an extensive clinical, biological and molecular characterization of an acute uratic inflammation mouse model which accurately mimics human gout. We report the efficacy of topical imiquimod treatment and its impact on Interferon-dependent down modulation of Il-1β gene expression in this experimental model.

Conclusion: Our work reveals several key features of MSU-dependent inflammation and identifies novel therapeutic opportunities for gout patients.

原理：尿酸单钠（MSU）晶体在痛风病理生理中的作用已得到很好的描述，IL-1β在构成该疾病标志的炎症反应中的主要作用也是如此。然而，尽管发现了NLRP3炎性体并将其作为模式识别受体的作用将体外检测危险信号（MSU）与IL-1β分泌联系起来，但导致痛风患者关节发炎的确切机制仍知之甚少。

方法：通过皮下注射小鼠MSU晶体获得急性尿酸盐晶体炎症。症状进行评分，通过ELISA和蛋白质印迹定量细胞因子，通过RT-qPCR和RNAseq进行基因表达。磁共振成像也用于评估炎症。

结果：我们提供了精确模拟人类痛风的急性尿道炎小鼠模型的广泛临床，生物学和分子表征。我们报告了局部咪喹莫特治疗的功效及其在此实验模型中对依赖干扰素的Il-1β基因表达下调的影响。

结论：我们的工作揭示了MSU依赖性炎症的几个关键特征，并为痛风患者确定了新的治疗机会。