【摘要】 目的用幽门螺杆菌诱导胃黏膜细胞AGS产生IFN-γ,探讨胃黏膜细产生IFN-γ的机制。方法用幽门螺杆菌感染胃黏膜细胞株AGS,用RT-PCR测定细胞表达IFN-γ的RNA,用ELISA法测定细胞产生的IFN-γ蛋白;用幽门螺杆菌的主要毒力CagA阳性质粒转染细胞,ELISA测定细胞产生的IFN-γ;CagA阳性质粒转染细胞后加入MeK/ErK、Src、P38和NF-kB的抑制剂,用ELISA测定细胞产生IFN-γ的变化。结果 AGS细胞感染幽门螺杆菌后可检测到IFN-γRNA和蛋白的表达,CagA阳性质粒转染细胞后引起IFN-γ蛋白的表达,MeK/ErK、P38和NF-kB引起IFN-γ表达量下降。结论幽门螺杆菌感染胃黏膜细胞AGS诱导产生IFN-γ,幽门螺杆菌的主要毒力CagA可诱导IFN-γ的产生,CagA诱导IFN-γ的产生依赖于MeK/ErK、P38和NF-kB三者参与的信号途径。更多还原

【Abstract】 Objective To determine if gastric epithelial cells produce IFN-γ and the mechanism of its production.Methods AGS gastric epithelial cells were infected with H.pylori and the production of IFN-γ was detected using RT-PCR and ELISA.AGS gastric epithelial cells were transfected with CagA plasmid and tested for IFN-γ using ELISA.MEK / ERK,Src,P38,and NF-kB inhibitors were then added to the cells transfected with CagA plasmid and they were tested for IFN-γ using ELISA.Results When AGS gastric epithelial cells were infected with H.pylori,the cells produced IFN-γ.When the cells were transfected with CagA plasmid,the cells also produced IFN-γ.When MeK/ErK,P38 and NF-kB inhibitors were added to the cells transfected with CagA plasmid,the production of IFN-γ was inhibited.Conclusion H.pylori AGS gastric epithelial cells to produce IFN-γ.As the main virulence factor for H.pylori,CagA induces cells to produce IFN-γ,and that production depends on signal pathways involving MeK / ErK,P38,and NF-kB.更多还原