甲型 H1N1 流感病毒感染小鼠的发病机制
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中国医学科学院医学实验动物研究所,卫生部人类疾病比较医学重点实验室,国家中医药管理局人类疾病动物模型三级实验室,北京 100021

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Pathogenesis of Influenza A(H1N1) Virus in Infected Mice
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Key Laboratory of Human Diseases Comparative Medicine,Ministry of Health; Institute of Medical Laboratory Animal Science,Chinese Academy of Medical Sciences; Key Laboratory of Human Diseases Animal Models,State Administration of Traditional Chinese Medicine,Beijing 100021,China

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    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-2IL-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。

    Abstract:

    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.

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鲍琳琳,孙惠惠,占玲俊,许黎黎,邓 巍,李枫棣,吕 琦,朱 华,秦 川.甲型 H1N1 流感病毒感染小鼠的发病机制[J].中国比较医学杂志,2011,21(2):16~20.

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  • 收稿日期:2010-10-12
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  • 在线发布日期: 2025-11-11
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