【摘要】 目的探讨原头蚴可能通过刺激巨噬细胞分泌KLF4而促使其向M2分化。方法原头蚴与RAW264.7细胞共培养,分别在12、36、48、84 h收集细胞和培养上清液,q RT-PCR检测KLF4、M1(Arg-1,Fizz-1,MR)、M2(TNF-α、IL-6、MCP-1)巨噬细胞因子的表达;ELISA检测相关因子分泌的含量。结果实验组(84 h)的KLF4 m RNA水平较对照组明显升高。随着感染时间延长,M2巨噬细胞的m RNA表达量及分泌含量呈上升趋势,M1巨噬细胞的m RNA表达量及分泌含量呈先升后降趋势。结论原头蚴刺激RAW264.7细胞,可能通过分泌某些抗原、蛋白,诱导巨噬细胞KLF4高表达而促使其向M2分化,抑制巨噬细胞的功能,从而逃逸宿主的免疫杀伤。更多还原

【Abstract】 This study was designed to explore whether Echinococcus granulosus stimulate macrophages tosecrete KLF4 and promote M2 differentiation of in RAW264.7. Firstly, RAW264.7 were cocultured with E.granulosus, then the macrophages and supernatant were collected at 12, 36, 48 and 84 hours for detecting therelative expression of KLF4, M1(Arg-1, Fizz-1, MR), M2(TNF-α, IL-6, MCP-1) m RNA by q RT-PCR; the levelsof cytokines in the cell culture supernatants were analyzed by ELISA. The expression levels of KLF4 in RAW264.7(84 h) of E. granulosus infected group were much higher than those in control group. With the infection timeprolonged, the m RNA expression and secretion of M2 in cell culture supernatants showed an upward trend, while them RNA expression and secretion of M1 in cell culture supernatants showed a rise trend firstly and then fall trend.Taken together, E. granulosus stimulate RAW264.7 to secret some protein antigen, to induce high levels of KLF4 and promote macrophages differentiation to M2, which may inhibit the function of macrophages, resulting inhost-immunity-defensive-system inhibition.更多还原