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首页> 外文期刊>Journal of inflammation. >Role of the NLRP3 inflammasome in the transient release of IL-1β induced by monosodium urate crystals in human fibroblast-like synoviocytes
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Role of the NLRP3 inflammasome in the transient release of IL-1β induced by monosodium urate crystals in human fibroblast-like synoviocytes

机译：NLRP3炎性小体在人成纤维样滑膜细胞中尿酸单钠晶体诱导的IL-1β瞬时释放中的作用

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Background To investigate whether monosodium urate (MSU) crystals induce interleukin (IL)-1β in human fibroblast-like synoviocytes (FLS), and whether the NLRP3 inflammasome is involved in the inflammatory mechanism. Methods Human FLS isolated from explants of synovial tissue were stimulated with MSU crystals (0.001 to 0.5 mg/ml) for different time course (6 hours to 48 hours). The expressions of IL-1β, IL-6, TNF-α and NLRP3 were evaluated with ELISA, Western blot and quantitative real-time PCR. Results Exposure of FLS to MSU crystals transiently induced a significant increase in IL-1β expression in culture medium with a peak at 6 h. The mRNA level of IL-1β in the FLS cells had a similar pattern at this time point. Changes in IL-6 and TNF-α expression were not observed. Simultaneously, intercellular pro-IL-1β was detected at 6 h. Furthermore, MSU crystals also induced NLRP3 mRNA and protein expression at 6 h to 48 h after MSU treatment. Conclusions MSU crystals directly increased IL-1β and intercellular NLRP3 expression in FLS cells. It is suggested that the NLRP3 inflammasome may be associated with IL-1β in FLS treated with MSU. Altogether, MSU could induce production and release of IL-1β through the NLRP3 inflammasome in human synoviocytes.
机译：背景研究尿酸单钠（MSU）晶体是否在人成纤维样滑膜细胞（FLS）中诱导白介素（IL）-1β，以及NLRP3炎性小体是否参与炎症机制。方法用滑膜组织外植体分离的人FLS用MSU晶体（0.001至0.5 mg / ml）刺激不同时间段（6小时至48小时）。用ELISA，Western blot和定量实时PCR检测IL-1β，IL-6，TNF-α和NLRP3的表达。结果FLS暴露于MSU晶体会瞬时诱导培养基中IL-1β表达的显着增加，并在6 h达到峰值。在这个时间点，FLS细胞中IL-1β的mRNA水平具有相似的模式。没有观察到IL-6和TNF-α表达的变化。同时，在6小时检测到细胞间前IL-1β。此外，MSU晶体在MSU处理后6 h至48 h也诱导NLRP3 mRNA和蛋白表达。结论MSU晶体直接增加FLS细胞中IL-1β和细胞间NLRP3的表达。提示NLRP3炎性体可能与MSU治疗的FLS中的IL-1β有关。总之，MSU可以通过人滑膜细胞中的NLRP3炎性小体诱导IL-1β的产生和释放。

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