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幽门螺杆菌感染小鼠胃黏膜组织细胞因子的水平变化 被引量:1

The change of gastric mucosal-associated cytokines in Helicobacter pylori infected mice
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摘要 目的检测幽门螺杆菌(Helicobacter pylori,H.pylori)感染小鼠后胃黏膜细胞因子的水平变化情况,分析机体的免疫应答状态。方法采用Real-Time-PCR法检测H.pylori感染小鼠后1、2、4及6周时胃黏膜H.pylori的定植数量及细胞因子(IFN-γ、IL-4、IL-10、IL-17A、Foxp3+)的mRNA表达水平,ELISA法测定胃黏膜IFN-γ、IL-4、IL-10、IL-17A的表达量。结果感染小鼠胃黏膜中H.pylori的定植量随着时间的推移在第4周达到高峰,第6周时有所下降。感染小鼠胃黏膜IFN-γ的mRNA水平明显高于PBS对照组,并随时间逐渐升高。IL-4及IL-10在感染6周内无明显变化,IL-17A和Foxp3+的mRNA水平在1、2周时无明显变化,第4周时显著上升,第6周时下降。感染小鼠胃黏膜IFN-γ、IL-4和IL-17A的蛋白水平变化在第1、2周时无明显变化,第4周时显著上升,第6周时下降,而IL-10变化不明显。结论 H.pylori早期感染可显著激发Th1和Th17应答,并伴随Treg细胞反应,这些可能与H.pylori逃避宿主免疫清除后的持续性感染有关。 With the aim to characterize the status of the immune responses post the Helicobacter pylori(H. pylori) infection, we analyzed the levels of gastric mucosal-associated cytokines. Using real-time PCR, the colonization of H. pylori was quantified and the levels of IFN-γ, IL-4, IL-10, IL-17A were detected on week 1, 2, 4, and 6 post the infection. The concentrations of gastric mucosal IFN-γ IL-4, IL-10 and IL-17A were determined by ELISA. The real-time PCR results showed that the colonization of H. pylori was gradually increased with the time in 4 weeks, and reduced at week 6; the mRNA levels of IFN-γ increased with the time in 4 weeks, and reduced at week 6. However, no significant changes were detected in IL-4 and IL-10, while IL-17A and Foxp3+ levels had no changes on week 1 and 2, but significantly increased on week 4, and reduced at week 6. The ELISA results showed that IFN-γ, IL-4 and IL-17A had no changes on week 1 and 2, but significantly increased in week 4, and reduced at week 6, while, IL-10 showed no significant change. All the results indicated that H. pylori could stimulate Thl and Thl7 responses in early period of infection, related to H. pylori immune evasion and persistent infections. accompanied by Treg cells responses, which might be
出处 《免疫学杂志》 CAS CSCD 北大核心 2014年第1期29-32,共4页 Immunological Journal
关键词 幽门螺杆菌 细胞因子 免疫应答 感染 Helicobacter pylori Cytokines Immune response Infection
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