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首页> 中文期刊> 《中国人兽共患病学报》 >幽门螺杆菌Tipα蛋白激活NLRP3炎性小体诱导THP-1细胞分泌IL-1β和IL-18

幽门螺杆菌Tipα蛋白激活NLRP3炎性小体诱导THP-1细胞分泌IL-1β和IL-18

         
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目的 以佛波酯(PMA)诱导分化的THP-1巨噬细胞为模型,探讨NLRP3炎性小体在幽门螺杆菌Tipα蛋白诱导炎性细胞因子分泌中的作用.方法 采用重组纯化Tipα蛋白刺激巨噬细胞,ELISA检测其促炎细胞因子TNF-α、IL-1β和IL-18的分泌水平.分别用NF-κB通路阻断剂PDTC和ROS清除剂NAC预处理细胞,ELISA检测预处理前后Tipα诱导细胞分泌促炎细胞因子水平差异,Western Blot检测NLRP3和Caspase-1分子的表达水平差异.结果 Tipα蛋白可显著诱导巨噬细胞产生TNF-α、IL-1β和IL-18;Tipα蛋白浓度为40 μg/mL时,刺激细胞6h后,TNF-α、IL-18和IL-1β表达水平接近峰值(P＜0.05).特异性阻断NF-κB信号通路后,巨噬细胞分泌的促炎细胞因子及Caspase-1和NLRP3分子的表达水平均较阻断前明显降低,ROS清除剂NAC预处理细胞后,巨噬细胞分泌的IL-18和IL-1β较处理前有明显降低(P＜0.05),TNF-α无明显变化;Western Blot结果显示Caspase-1和NLRP3分子的表达水平较阻断前均有明显降低.结论 Tipα能够促进巨噬细胞产生促炎细胞因子IL-1β和IL-18;NLRP3/Caspase-1途径可能参与了Tipα诱导的IL-1β和IL-18分泌.%We preliminarily investigated the role of NLRP3 inflammasome in Helicobacter pylori (H.pylori) Tipa-induced pro-inflammatory cytokines secretion in PMA-differentiated human acute monocytic leukemia cell line THP-1.PMA-differentiated THP-1 cells were treated with pure recombinant Tips protein.The secretion levels of TNF-α,IL-1β and IL-18 in supernatant of culture medium were detected by ELISA.Then we blocked MyD88/NF-κB and NLRP3/Caspase-1 pathways by PDTC or the general ROS scavenger,NAC,respectively,and determined the secretion levels of proinflammatory cytokines and the expression levels of NLRP3 and Caspase-1.The results showed that Tips protein can significantly induced the secretion of TNF-α,IL-1β and IL-18 in THP-1 cells in a time and dose-dependent manner.Levels of TNF-α,IL-1β and IL-18 approached their peaks at 6 h post-treatment by 40 μg/mL of Tipα protein (P＜0.05).Moreover,the blockade of NF-κB signaling pathway by PDTC can inhibit the secretion of proinflammatory cytokines and the expression of NLRP3 and Caspase-1.When THP-1 cells were pre-treated with ROS scavenger NAC,the Tipα-induced increased IL-1β and IL-18 secretion was obviously eliminated (P＜0.05),while TNF-α level had no significant difference,and the expression levels of Caspase-1 and NLRP3 also have a significant decrease.Our results demonstrated that Tipα can promote THP-1-drived macrophages to secrete proinflammatory cytokines TNF-α,IL-1β and IL-18,and the NLRP3/Caspase-1 pathway may be involved in the Tipα protein-induced IL-1β and IL-18 secretion.

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