摘要
目的研究肺炎支原体脂质相关膜蛋白对巨噬细胞分泌细胞因子和诱导巨噬细胞凋亡的影响,初步探讨肺炎支原体引起动脉粥样硬化的机制。方法用ELISA检测肺炎支原体脂质相关膜蛋白诱导体外培养的巨噬细胞培养上清液中TNF-α、IL-1β和IL-6的含量;用流式细胞术检测脂质相关膜蛋白诱导巨噬细胞的凋亡率;West-ern blot方法检测经脂质相关膜蛋白作用的巨噬细胞NF-κB的激活和NF-κB抑制剂吡咯啉烷二甲基硫脲对巨噬细胞分泌细胞因子和诱导巨噬细胞凋亡的影响。结果脂质相关膜蛋白能促进巨噬细胞分泌高水平的TNF-α、IL-1β和IL-6和发生凋亡;并能使NF-κB从细胞浆中转位到细胞核内;吡咯啉烷二甲基硫脲能显著抑制巨噬细胞NF-κB的激活,且能抑制脂质相关膜蛋白诱导的巨噬细胞分泌细胞因子和发生凋亡。结论肺炎支原体脂质相关膜蛋白可通过激活NF-κB诱导巨噬细胞分泌前炎症细胞因子和促进凋亡,可能在动脉粥样硬化的发病中起重要作用。
Aim To study the proinflammatory cytokines production and apoptosis of macrophages upon Myco- plasma pneumoniae （M. pneumoniae） lipid-associated membrane proteins （LAMP） stimulation, and evaluate the molecular mechanism of M. pneumoniae to cause atherosclerosis. Methods The cultured human macrophages were incubated with various concentrations of M. pneumoniae LAMP preparations. The proinflammatory cytokines TNF-α, IL-1β and IL-6 production were detected by ELISA and cell apoptosis by flow cytometry. At the same time, the activation of NF-kB and the effects of pyrrolidine dithiocarbamate （ PDTC）, an inhibitor of NF-kB, on M. pneumoniae LAMP-induced macrophages apoptosis were analyzed by Western blot. Results M. pneumoniae LAMP could induce high level of TNF-α, IL-1β and IL-6 production and macrophages apoptosis. These effects were highly associated with NF-KB activation of macropha- ges. PDTC could significantly inhibit the activation of NF-KB and partially reduce M. pneumoniae LAMP-induced macro- phages secretion and apoptosis. Conclusions M. pneumoniae LAMP can induce proinflammatory cytokines secretion and macrophages apoptosis by activating NF-kB, and it may be an important etiological factor for atherosclerosis.
出处
《中国动脉硬化杂志》
CAS
CSCD
北大核心
2012年第9期773-776,共4页
Chinese Journal of Arteriosclerosis
基金
国家自然科学基金项目(81072418)
湖南省教育厅优秀青年基金项目(09B088)
湖南省高校科技创新团队资助项目(湘教通[2010]212号)
关键词
肺炎支原体
脂质相关膜蛋白
前炎症因子
细胞凋亡
动脉粥样硬化
Mycoplasma Pneumoniae
Lipid-Associated Membrane Proteins
Proinflammatory Cytokines
Cell Ap- optosis
Atherosclerosis
