甲型H1N1流感病毒感染小鼠的发病机制

Pathogenesis of Influenza A(H1N1) Virus in Infected Mice

目的甲型H1N1流感病毒A/California/7/2009感染BALB/c小鼠,研究甲型H1N1流感病毒病毒性肺炎发病机制。方法 4～6周龄雌性BALB/c小鼠60只,随机分为2组,实验组和对照组,每组30只。CA7流感病毒滴鼻制备甲流病毒感染小鼠模型。攻毒后第5天解剖实验和对照组小鼠,取肺组织,测定肺组织中IL-2,IL-6,TNF-α含量。结果结果实验组肺组织中IL-6,TNF-α,水平明显高于对照组,IL-2水平明显低于对照组,差异均有显著性(P<0.05)。结论 IL-6、TNF-α、IL-2这3种细胞因子在感染甲流病毒后的显著性变化与病毒感染后的肺组织病理损伤有密切的关系。

Objective To study the mechanism of the influenza virus infection in BALB/c mice with A/ California/7/2009Influenza H1N1 virus.Methods Sixty BALB/c mice were randomly divided into 2 groups：experimental group and control group,each group consisted of 30 mice.The CA7 influenza virus was used to establish influenza models.The expressions of lung IL-6,TNF-α,and IL-2 in experimental group of 5th day control group were detected by enzyme linked immunosorbent assay（ELISA）.Results The lung tissue IL-6,TNF-α levels were significantly higher,IL-2 levels were significantly lower than that in the control group,the differences were significant（P 0.05）.Conclusions The cytokines IL-2,IL-6 and TNF-α may participate in the whole process of influenza A H1N1 virus infection and their lung levels are positively correlated with the severity of the disease.