TLR在甲型流感病毒性脑炎中的分子机制研究  

Molecular mechanism of TLR in viral encephalitis after infection of influenza A virus

作　　者：王司晔[1] 王雨薇 郭爱松[1] WANG Siye;WANG Yuwei;GUO Aisong(Department of Rehabilitation Medicine,the Affiliated Hospital of Nantong University,Jiangsu 226001;Medicine School of Nantong University)

机构地区：[1]南通大学附属医院康复医学科,江苏226001 [2]南通大学医学院

出　　处：《交通医学》2019年第5期438-440,444,共4页Medical Journal of Communications

基　　金：国家自然科学基金青年项目(81601752)

摘　　要：目的:探讨Toll样受体(TLR)在甲型流感病毒感染导致的病毒性脑炎发病中的分子机制和信号通路。方法:选择具有嗜中枢神经系统性的甲型流感病毒株(A/WSN/33,H1N1)建立小鼠病毒性脑炎模型,观察小鼠生存和体重曲线,检测小鼠脑组织中TLR3和TLR7蛋白表达。结果:感染组小鼠从感染后第4天起开始出现死亡个例,感染后第6天死亡3例,最多,生存率由80%降至50%。感染第7天以后至14天,生存率保持在40%。对照组小鼠体重平稳上升,感染组小鼠从感染后第2天起体重呈下降趋势,观察期结束时体重为12.67±0.58 g,低于对照的14.11±0.5 g,差异有统计学意义(P<0.05)。WSN病毒感染小鼠后第6天,感染组小鼠脑组织中TLR3和TLR7蛋白表达高于对照组,差异均有统计学意义(P<0.05)。结论:TLR家族在甲型流感病毒导致的病毒性脑炎的发病机制中可能起到调节信号通路的作用。Objective:To investigate the molecular mechanism and the signaling pathway of toll-like receptor(TLR)in viral encephalitis caused by influenza A virus infection,and to provide theoretical basis for effective prevention and treatment of such diseases.Methods:Influenza A virus strain(WSN/33,H1N1)which has an affinity for the central nervous system was selected to establish a viral encephalitis model in mice.The survival curves and body mass index of the mice were analyzed,and the protein expression of TLR3 and TLR7 in mouse brain tissue was detected.Results:In the infected group,the mice began to die on the 4th day after infection,and 3 mice died on the 6th day after infection,with the highest survival rate reduced from 80%to 50%.From 7 to 14 days after infection,the survival rate remained at 40%.The weight of mice in the control group grew up steadily,while that of mice in the infection group showed a decreasing trend from the second day after infection.At the end of the observation period,the weight was 12.67±0.58 g,lower than that in the control group(14.11±0.5 g),with statistically significant difference(P<0.05).On the 6th day after WSN virus infected mice,the expression levels of TLR3 and TLR7 in the brain tissues of mice in the infected group increased to different degrees compared with those in the control group,and both of them were statistically significant(P<0.05).Conclusion:TLR family may play a role in regulating signaling pathways in the pathogenesis of viral encephalitis caused by influenza A virus.

关 键 词：病毒性脑炎 甲型流感病毒 TOLL样受体 分子机制 信号通路 

分 类 号：R512.3[医药卫生—内科学]