Serial histopathological examination of the lungs of mice infected with influenza A virus PR8 strain.
Serial histopathological examination of the lungs of mice infected with influenza A virus PR8 strain.
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DOI：
10.1371/journal.pone.0021207
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发表时间：
2011
期刊：
影响因子：
3.7
通讯作者：
Kudo K
中科院分区：
文献类型：
--
作者：
Fukushi M;Ito T;Oka T;Kitazawa T;Miyoshi-Akiyama T;Kirikae T;Yamashita M;Kudo K
已知禽流感H5 N1和2009年大流行性（H1N1）病毒可诱导病毒性肺炎和随后的急性呼吸窘迫综合征（ARDS）伴弥漫性肺泡损伤（DAD）。ARDS/DAD的死亡率极高，约为60%，并且尚未建立有效的治疗方法。我们检测了流感病毒感染小鼠肺部的一系列病理变化，以确定从病毒性肺炎到ARDS/DAD的进展。用流感A/波多黎各/8/34（PR 8）病毒鼻内感染小鼠，并且每2天对它们的肺进行宏观和微观病理学检查。我们还评估了一般状况、存活率、体重、肺中的病毒载量和血清中的表面活性蛋白。结果，所有感染小鼠在感染后9天内死亡。感染后2天，肺泡隔炎症，即，细支气管周围观察到间质性肺炎。感染后4 ~ 6天，间质性肺炎伴肺泡萎陷扩展至整个肺。感染后6 ~ 9天，所有濒死和死亡小鼠肺内均出现DAD，并伴有严重肺泡萎陷。相反，在感染后2至6天的活感染小鼠中未观察到DAD，尽管它们的一般状况较差。此外，在20天的观察期内，对感染PR 8病毒的小鼠进行了组织病理学分析，该剂量为小鼠致死剂量的50%。在所有死亡小鼠中观察到DAD伴肺泡塌陷。然而，在存活小鼠中，在其肺部广泛观察到腺化生而不是DAD。目前的研究表明，DAD与严重的肺泡萎陷是与死亡的小鼠流感病毒感染模型。抑制DAD伴肺泡萎陷的发展可能降低流感病毒感染引起的重症病毒性肺炎的死亡率。
Avian influenza H5N1 and pandemic (H1N1) 2009 viruses are known to induce viral pneumonia and subsequent acute respiratory distress syndrome (ARDS) with diffuse alveolar damage (DAD). The mortality rate of ARDS/DAD is extremely high, at approximately 60%, and no effective treatment for ARDS/DAD has been established. We examined serial pathological changes in the lungs of mice infected with influenza virus to determine the progress from viral pneumonia to ARDS/DAD. Mice were intranasally infected with influenza A/Puerto Rico/8/34 (PR8) virus, and their lungs were examined both macro- and micro-pathologically every 2 days. We also evaluated general condition, survival rate, body weight, viral loads in lung, and surfactant proteins in serum. As a result, all infected mice died within 9 days postinfection. At 2 days postinfection, inflammation in alveolar septa, i.e., interstitial pneumonia, was observed around bronchioles. From 4 to 6 days postinfection, interstitial pneumonia with alveolar collapse expanded throughout the lungs. From 6 to 9 days postinfection, DAD with severe alveolar collapse was observed in the lungs of all of dying and dead mice. In contrast, DAD was not observed in the live infected-mice from 2 to 6 days postinfection, despite their poor general condition. In addition, histopathological analysis was performed in mice infected with a dose of PR8 virus which was 50% of the lethal dose for mice in the 20-day observation period. DAD with alveolar collapse was observed in all dead mice. However, in the surviving mice, instead of DAD, glandular metaplasia was broadly observed in their lungs. The present study indicates that DAD with severe alveolar collapse is associated with death in this mouse infection model of influenza virus. Inhibition of the development of DAD with alveolar collapse may decrease the mortality rate in severe viral pneumonia caused by influenza virus infection.
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影响因子：
2.7
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DOI：
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发表时间：
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发表时间：
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影响因子：
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通讯作者：
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