IFN-γ在沙眼衣原体呼吸道感染中免疫防御机制的探讨

目的:检测与IFN-γ作用相关的酶吲哚胺2,3二氧化酶(IDO)、诱导性一氧化氮合成酶(iNOS)和NADPH氧化酶(ox)gp91在沙眼衣原体呼吸道感染中的表达及与机体防御的关系,探讨衣原体感染中IFN-γ免疫防御作用的机制.方法:用沙眼衣原体小鼠肺炎株(MoPn)通过鼻腔感染C57BL/6(H-2b)小鼠,用过氧化物酶连接的鼠抗衣原体脂多糖单抗染色HeLa 229细胞,检测衣原体在肺组织的生长;用RT-PCR检测衣原体感染后第7及14天小鼠肺组织IFN-γ、IDO、iNOS和gp91NADPH ox mRNA表达.结果:MoPn呼吸道感染后小鼠肺组织匀浆衣原体活性测定,于感染后第2天,HeLa 229细胞内可见有衣原体包涵体生长,IFU值增高,于感染后第7天IFU达最高水平,以后逐渐下降,至感染后21天基本恢复到基线水平.与未感染的对照组比较,Th1细胞因子IFN-γ于感染后第7天表达显著增高,感染后14天有所降低,但仍维持较高水平;同时衣原体感染可显著诱导与IFN-γ作用相关的三种酶IDO、iNOS和gp91 NADPH ox在小鼠肺组织的表达,感染后第7及14天,IDO,iNOS及gp91 NADPH ox的表达与对照组比较均有显著差异,其中IDO和gp91 NADPH ox于感染后第7天mRNA表达增高显著(P＜0.01),14天略有下降(P＜0.05).结论:衣原体呼吸道感染诱导Th1细胞因子IFN-γ mRNA高表达,参与宿主对衣原体的清除及机体免疫防御,此作用可能与其相应的酶IDO、iNOS和gp91 NADPH ox表达增高有关.     

沙眼衣原体感染免疫反应的研究进展

沙眼衣原体(Chlamydia trachomatis,Ct)是一类严格寄生于真核细胞内的原核细胞型微生物,是沙眼和性传播疾病中最常见的病原体。据统计,全世界每年有5亿人患沙眼,其中700～900万人失明,沙眼是引起失明最重要的原因之一。沙眼衣原体另外一个重要的危害是它还引起泌尿生殖道感染,并通过性接触传播,是性病中最多见的病原体,可引起男性尿道炎、附睾炎,女性宫颈炎、盆腔炎,不育等,更可引起新生儿的结膜炎、肺炎,影响下一代的健康,     

活化血小板参与缺血性脑卒中炎症反应机制初探

目的 通过细胞共培养模型初步探讨活化血小板参与缺血性脑卒中炎症反应的机制.方法 分离健康人血小板,以0.8μmol/L二磷酸腺苷(ADP)作用20 min激活.同时设静息血小板做为对照,应用血细胞分析仪检测血小板平均内含物(MAC)浓度;将静息血小板和活化血小板分别与人脐静脉内皮细胞株共培养12 h,同时设ADP对照组(只加入等量ADP,无血小板)和空白对照组,采用RT-PCR法检测人脐静脉内皮细胞炎性细胞因子白介素-1β(IL-1β)、白介素.6(IL-6)、白介素-8(IL-8)、单核细胞趋化蛋白-1(MCP-1)的mRNA表达情况.结果与静息血小板组[(266.80±22.14)g/L]比较,ADP诱导激活的活化血小板MPC值[(231.90±14.63)g/L]减低,差异有统计学意义(P<0.05);RT-PCR检测结果显示活化血小板可以诱导共培养的人脐静脉内皮细胞表达IL-1β、IL-6、IL-8、MCP-1 mRNA,而静息血小板组、ADP对照组和空白对照组均无上述细胞因子的表达.结论 体外活化的血小板能够启动血小板一内皮细胞反应,诱导其表达炎症细胞因子,是缺血性脑卒中炎症反应发生的可能机制之一.     

活化血小板参与缺血性脑卒中炎症反应机制初探

Objective To preliminarily study the role of activated platelets in inflammatory response in ischemic stroke by using the platelet and vascular endothelial cell co-culture model.Methods Platelets were isolated from healthy donator's peripheral blood and activated in vitro by 0.8 μmol/L ADP in ischemic stroke; resting platelets were also chosen.The mean platelet component (MPC)concentration was measured by hematology analyzer.Resting platelets and activated platelets were co-cultured with vascular endothelial cells for 12 h,respectively; the other 2 control groups (ADP only,blank) were employed in the experiment.RT-PCR was used to detect the expression level of mRNA of proinflammatory cytokines in the endothelial cells,including IL-1β,IL-6,IL-8 and MCP-1.Results Compared with the resting platelets[(266.80±22.14) g/L],ADP-induced activated platelets[(231.90±14.63) g/L]showed significantly lower concentration of MPC (P<0.05).Activated platelets in the co-culture model could induce the mRNA expression of IL-1β,IL-6,IL-8 and MCP-1 in the endothelial cells,while resting platelets could not.Conclusion Activated platelets can trigger an interaction between platelets and endothelial cells in vitro,and induce the mRNA expression of proinflammatory cytokines in the endothelial cells,which may be one of the mechanisms of inflammatory response in iscbemic stroke.     

活化血小板参与缺血性脑卒中炎症反应机制初探

Objective To preliminarily study the role of activated platelets in inflammatory response in ischemic stroke by using the platelet and vascular endothelial cell co-culture model.Methods Platelets were isolated from healthy donator's peripheral blood and activated in vitro by 0.8 μmol/L ADP in ischemic stroke; resting platelets were also chosen.The mean platelet component (MPC)concentration was measured by hematology analyzer.Resting platelets and activated platelets were co-cultured with vascular endothelial cells for 12 h,respectively; the other 2 control groups (ADP only,blank) were employed in the experiment.RT-PCR was used to detect the expression level of mRNA of proinflammatory cytokines in the endothelial cells,including IL-1β,IL-6,IL-8 and MCP-1.Results Compared with the resting platelets[(266.80±22.14) g/L],ADP-induced activated platelets[(231.90±14.63) g/L]showed significantly lower concentration of MPC (P<0.05).Activated platelets in the co-culture model could induce the mRNA expression of IL-1β,IL-6,IL-8 and MCP-1 in the endothelial cells,while resting platelets could not.Conclusion Activated platelets can trigger an interaction between platelets and endothelial cells in vitro,and induce the mRNA expression of proinflammatory cytokines in the endothelial cells,which may be one of the mechanisms of inflammatory response in iscbemic stroke.