Zeng Mei, Dang Wantai, Chen Baofeng, Qing Yufeng, Xie Wenguang, Zhao Mingcai, Zhou Jingguo
Biology Group, North SiChuan Medical College, 1# Fujiang Road, Nanchong, 637000, Sichuan, China.
Institute of Rheumatology and Immunology, Department of Rheumatology and Hematology, The Affiliated Hospital of North Sichuan Medical College, 63 Wenhua Road, Nanchong, 637000, Sichuan, China.
Clin Rheumatol. 2016 Sep;35(9):2251-8. doi: 10.1007/s10067-015-3109-5. Epub 2015 Nov 7.
Acute gouty arthritis (AGA) is an auto-inflammatory disease characterized by resolving spontaneously, which suggests that negative feedback loops control inflammatory and immunological responses to monosodium urate (MSU) crystals. By now, the molecular mechanism for spontaneous resolution of acute GA remains unclear; this study was undertaken to evaluate whether IL-37 is involved in spontaneous resolution of AGA. A total of 45 acute GA (AGA),29 non-acute GA (NAGA) male patients and 82 male health control (HC) were involved in this study, we measured IL-7 expression in the peripheral blood mononuclear cells (PBMCs), together with levels of IL-1β, IL-6, IL-10, TNF-α and TGF-β1 in the serum. Further, we either inhibited IL-37 expression in human PBMCs with siRNA or over-expressed the cytokine in human macrophages. Pro-inflammatory cytokine IL-1β, IL-6, and TNF-α expressions were significantly higher in the AGA group than in the NAGA or HC group (P < 0.05, respectively). However, anti-inflammatory IL-37, TGF-β1, and IL-10 were greater in the NAGA group than in the AGA and HC groups (P < 0.05, respectively). Expression of IL-37 in MSU crystal-treated macrophages inhibited the expression of pro-inflammatory cytokines, whereas the abundance of these cytokines increased with silencing of endogenous IL-37 in human blood cells. However, anti-inflammatory TGF-β1 and IL-10 expressions in these supernatants were unaffected by over-expression or knockdown of IL-37. Our study indicates that IL-37 is an important anti-inflammatory cytokine in AGA by suppressing the production of pro-inflammatory cytokines. Thus, IL-37 may provide a novel research target for the pathogenesis and therapy of GA.
急性痛风性关节炎(AGA)是一种以自发缓解为特征的自身炎症性疾病,这表明负反馈回路控制着对尿酸单钠(MSU)晶体的炎症和免疫反应。目前,急性痛风性关节炎自发缓解的分子机制尚不清楚;本研究旨在评估白细胞介素-37(IL-37)是否参与急性痛风性关节炎的自发缓解。本研究共纳入45例急性痛风性关节炎(AGA)男性患者、29例非急性痛风性关节炎(NAGA)男性患者和82例男性健康对照者(HC),我们检测了外周血单个核细胞(PBMCs)中IL-37的表达,以及血清中IL-1β、IL-6、IL-10、肿瘤坏死因子-α(TNF-α)和转化生长因子-β1(TGF-β1)的水平。此外,我们用小干扰RNA(siRNA)抑制人PBMCs中IL-37的表达,或在人巨噬细胞中过表达该细胞因子。促炎细胞因子IL-1β、IL-6和TNF-α在AGA组中的表达明显高于NAGA组或HC组(分别为P<0.05)。然而,抗炎性细胞因子IL-37、TGF-β1和IL-10在NAGA组中的水平高于AGA组和HC组(分别为P<0.05)。MSU晶体处理的巨噬细胞中IL-37的表达抑制了促炎细胞因子的表达,而这些细胞因子的丰度随着人血细胞中内源性IL-37的沉默而增加。然而,这些上清液中抗炎性细胞因子TGF-β1和IL-10的表达不受IL-37过表达或敲低的影响。我们的研究表明,IL-37通过抑制促炎细胞因子的产生,是急性痛风性关节炎中一种重要的抗炎细胞因子。因此,IL-37可能为痛风性关节炎的发病机制和治疗提供一个新的研究靶点。