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石连杰, 李建红, 岑筱敏等. 类风湿关节炎中CCL19/IL-1β正反馈环路的体外实验[J]. koko体育app 学报（医学版）, 2015, 46(2): 272-275.
引用本文: 石连杰, 李建红, 岑筱敏等. 类风湿骨痛髋骨关节炎中CCL19/IL-1β正反面馈环路的休外實驗[J]. 湖北院校学报（药学版）, 2015, 46(2): 272-275.
SHI Lian-jie, LI Jian-hong, CEN Xiao-min. et al. CCL19/IL-1β Positive Feedback Loop Involved in the Progress of Inflammation in Rheumatoid Arthritis[J]. Journal of Sichuan University (Medical Sciences), 2015, 46(2): 272-275.
Citation: SHI Lian-jie, LI Jian-hong, CEN Xiao-min. et al. CCL19/IL-1β Positive Feedback Loop Involved in the Progress of Inflammation in Rheumatoid Arthritis[J]. Journal of Sichuan University (Medical Sciences), 2015, 46(2): 272-275.

类风湿关节炎中CCL19/IL-1β正反馈环路的体外实验

CCL19/IL-1β Positive Feedback Loop Involved in the Progress of Inflammation in Rheumatoid Arthritis

  • 摘要: 目的 探讨趋化因子（C-C基序）配体19（CCL19）在类风湿关节炎发病中的功能及机制。 方法 收集5例类风湿关节炎患者的滑膜细胞，另采用密度梯度离心法分离出5例健康人外周血单个核细胞（PBMCs），对两种细胞分别给予白细胞介素（IL）-1β、肿瘤坏死因子-α（TNF-α）、IL-17等细胞因子刺激，实时定量PCR检测细胞中\CCL19和其受体\CCR7基因的表达。同时，采用不同浓度的CCL19处理滑膜细胞和PBMCs，实时定量PCR检测细胞中\IL-1β、TNF-α及\CCR7的表达改变。利用Western blot技术检测不同浓度CCL19处理后的PBMCs中磷酸化的脑外信号调节激酶（p-ERK）、磷酸化p38(p-p38）的表达情况。 结果 IL-1β和TNF-α能促进滑膜细胞和PBMCs中\CCL19/\CCR7的表达，并具有协同效应；CCL19能促进滑膜细胞和PBMCs中\IL-1β、TNF-α和CCR7的表达；CCL19可以活化PBMCs中的p-ERK和p-p38。 结论 CCL19可能通过活化p-ERK和p-p38上调IL-1β表达，而高表达的IL-1β通过正反馈进一步促进CCL19的表达参与类风湿关节炎疾病的发生发展。  
    Abstract: Objective To explore the function and mechanism of CCL19 in the pathogenesis of rheumatoid arthritis. Methods Synovial fibroblasts were collected from 5 cases of rheumatoid arthritis. Peripheral blood mononuclear cells (PBMCs) were obtained from 5 healthy people by Ficoll-Hypaque density gradien centrifugation. The cells were stimulated with IL-1β, TNF-α, IL-17 and other cytokines, and then the expression of CCL19 was detected by RT-PCR. The cells also were treated with different concentration of CCL19, then the expressions of IL-1β, TNF-α were detected by RT-PCR, the expressions of p-ERK, p-p38 were detected by western blot. Results IL-1β promoted the CCL19/CCR7 expression in both synovial fibroblasts and PBMCs. CCL19 upregulated the expression of IL-1β in both synovial fibroblasts and PBMCs. The stimulation of CCL19 also increased its receptor CCR7 expression. CCL19 activated p-ERK and p-p38 in PBMCs. Conclusion The positive feedback loop between CCL19 and IL-1β participate in the development of rheumatoid arthritis.  
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