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作 者:王建军[1] 王泽友[1] 姚永良[1] 吴建红[1] 李光新[2]
机构地区:[1]江苏大学附属昆山医院检验科,昆山215300 [2]重庆市肿瘤研究所病理科,重庆215300
出 处:《中国免疫学杂志》2015年第6期737-740,共4页Chinese Journal of Immunology
基 金:昆山市科学与技术项目(No.KS1347);江苏大学医学临床科技发展基金项目(JYL-20140047)
摘 要:目的:探讨幽门螺杆菌(Helicobacter pylori,H.pylori)作用巨噬细胞后导致的细胞炎症反应机制及对宿主巨噬细胞的损伤作用。方法:ELISA方法检测幽门螺杆菌感染巨噬细胞后细胞培养上清液中细胞因子IL-23、IL-10、TNF-α及IL-8的含量,Western blot分析幽门螺杆菌作用巨噬细胞后细胞胞内蛋白NOS2、COX2的表达水平;同时流式细胞技术分析幽门螺杆菌处理巨噬细胞后对细胞的凋亡作用。结果:细胞因子IL-23、IL-10、TNF-α、IL-8在幽门螺杆菌作用巨噬细胞后细胞培养上清中分泌显著增多(P<0.05),且NOS2、COX2蛋白表达显著增强(P<0.03);幽门螺杆菌处理巨噬细胞后巨噬细胞凋亡显著增多(P<0.05)。结论:幽门螺杆菌作用巨噬细胞后诱导巨噬细胞增强炎症反应而抑制或杀伤幽门螺杆菌,同时长时间作用能诱导宿主巨噬细胞凋亡。Objective: To explore the inflammatory responses of macrophages treated with Helicobacter pylori. Methods: Cytokines IL-23,IL-10,TNF-α and IL-8 in cell culture supernatant of macrophages stimulated with Helicobacter pylori were determined by ELISA kits,and the expression of intracellular proteins NOS2 and COX2 in Helicobacter pylori treated macrophages was analyzed by Western blot. Then,the apoptosis of Helicobacter pylori stimulated macrophages was detected by flow cytometry. Results: The secretion of cytokines IL-23,IL-10,TNF-α and IL-8 in the culture supernatant of Helicobacter pylori treated macrophages increased significantly( P〈0. 05),and the expression of NOS2 and COX2 was enhanced evidently( P〈 0. 05). Meanwhile,helicobacter pylori could induce the apoptosis of macrophages obviously( P 0. 03). Conclusion: The inflammatory responses of macrophages treated with Helicobacter pylori would be promoted to inhibit or kill Helicobacter pylori,furthermore,Helicobacter pylori could induce the apotosis of macrophages.
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