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机构地区:[1]宁夏医科大学总医院神经内科,宁夏颅脑疾病重点实验室-省部共建国家级重点实验室培育基地,宁夏银川750004
出 处:《细胞与分子免疫学杂志》2011年第10期1083-1085,共3页Chinese Journal of Cellular and Molecular Immunology
基 金:2007年国家自然科学基金面上项目(30760067);教育部春晖计划(Z2008-1-75002);宁夏医科大学"博士学位建设学科"开放课题(KF2010-34)
摘 要:目的:了解在体外培养条件下丙型肝炎病毒(HCV)刺激小鼠小胶质细胞(BV2)后Toll样受体9(TLR9)蛋白的表达变化及其对MCP-1(人单核细胞趋化蛋白-1)和TNF-α分泌的影响,探讨HCV感染中枢神经系统(CNS)后小胶质细胞TLR9蛋白的表达及其相应细胞因子的变化。方法:体外培养BV2细胞,分为HCV阳性血清组、正常人血清组、空白对照组。每组各20例细胞样本。在12h收集细胞和上清液,用流式细胞术检测TLR9蛋白的表达,ELISA法检测培养上清中MCP-1和TNF-α的含量,并应用SPSS11.0统计软件包进行统计学分析。结果:(1)各组BV2细胞均有TLR9蛋白的表达,HCV阳性血清组中TLR9蛋白的表达高于正常人血清组、空白对照组(P<0.01);正常人血清组和空白对照组无统计学差异(P>0.05);(2)HCV阳性血清组MCP-1和TNF-α含量高于正常人血清组、空白对照组(P<0.01);且HCV阳性血清组TLR9蛋白的表达量与MCP-1和TNF-α的分泌可能呈正相关。结论:HCV阳性血清刺激可使体外培养的BV2细胞表达TLR9蛋白增高,且可能诱导了MCP-1和TNF-α的分泌。TLR9蛋白可能参与了HCV在中枢神经系统感染中的早期固有免疫应答。AIM: To detect TLR9 expression and its effect on the secretion of MCP-1 and TNF-α after mouse microglia (BV2) were infected by hepatitis C virus (HCV), and to explore the mechanism of HCV-induced central nervous system (CNS) infection. METHODS: BV2 cells were cultured in vitro and divided into a HCV-positive serum group, a normal serum group (negative control) and a blank control group, with each group of 20 samples. The cells and the supernatants were collected at 12 h, detected for TLR9 expression by flow cytometry (FCM), and determined for the levels of TNF-α and MCP-1 by ELISA. Then the data was statistically analyzed by SPSS11.0. RESULTS: (1) FCM showed TLR9 expression in all three groups, with the strongest expression in the HCV-positive serum group (P〈0.01), while there was no statistical significance between the normal serum group and the blank control group (P〉0.05). (2) The levels of TNF-α and MCP-1 in the HCV-positive serum group were higher than those in the other groups (P〈0.01), which correlated with enhanced TLR9 expression in the HCV-positive serum group. CONCLUSION: HCV-positive serum causes enhanced TLR9 expression and the secretion of MCP-1 and TNF-α. in BV2 cells, suggesting the involvement of TLR9 in the early inherent immune response triggered by HCV-induced CNS infection.
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