Kawaguchi Akira, Suzuki Tadaki, Ohara Yuki, Takahashi Kenta, Sato Yuko, Ainai Akira, Nagata Noriyo, Tashiro Masato, Hasegawa Hideki
Department of Pathology, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan.
Center for Influenza Virus Research, National Institute of Infectious Diseases, Musashimurayama, Tokyo, Japan.
PLoS One. 2017 Feb 28;12(2):e0173008. doi: 10.1371/journal.pone.0173008. eCollection 2017.
Influenza A virus is the respiratory pathogen responsible for influenza. Infection by the 2009 pandemic influenza A (H1N1) virus caused severe lower airway inflammation and pneumonia. Asthma is a chronic inflammatory disorder of the airways that affects the entire brachial tree, and was one of the commonest underlying medical conditions among patients hospitalized with the 2009 pandemic influenza virus infection. Although respiratory virus infections are the major causes of asthma exacerbation, the mechanism by which influenza exacerbates asthma is poorly understood. Animal models of disease comorbidity are crucial to understanding host-pathogen interactions and elucidating complex pathologies. Existing murine models of influenza virus infection in asthmatics show that asthmatic mice are highly resistant to influenza virus infection, which contradicts clinical observations in humans. Here, we developed a murine model of influenza virus/asthma comorbidity using NC/Nga mice, which are highly sensitive to allergic reactions such as atopic dermatitis and allergic airway inflammation. This model was then used to examine the impact of allergic airway inflammation on lung pathology in the 2009 pandemic influenza virus infected mice. The results showed that induction of acute allergic airway inflammation in pre-existing influenza virus infection had additive effects on exacerbation of lung pathology, which mirrors findings in human epidemiological studies. In contrast, pre-existing allergic airway inflammation protected from subsequent influenza virus infection, which was compatible with those of previous murine models of influenza virus infection in asthmatic mice. These variable outcomes of this murine model indicate that the temporal relation between allergic airway inflammation and influenza virus infection might play a critical role in asthma and influenza comorbidity. Thus, this murine model will further our understanding of how influenza virus infection affects an asthmatic host and may aid the development of strategies to improve treatments and outcomes for asthmatics harboring influenza virus infection.
甲型流感病毒是引起流感的呼吸道病原体。2009年甲型H1N1大流行性流感病毒感染可导致严重的下呼吸道炎症和肺炎。哮喘是一种影响整个支气管树的气道慢性炎症性疾病,是2009年甲型H1N1大流行性流感病毒感染住院患者中最常见的基础疾病之一。虽然呼吸道病毒感染是哮喘加重的主要原因,但流感加重哮喘的机制尚不清楚。疾病共病的动物模型对于理解宿主-病原体相互作用和阐明复杂病理至关重要。现有的哮喘患者甲型流感病毒感染小鼠模型显示,哮喘小鼠对甲型流感病毒感染具有高度抗性,这与人类临床观察结果相矛盾。在此,我们利用对特应性皮炎和过敏性气道炎症等过敏反应高度敏感的NC/Nga小鼠,建立了甲型流感病毒/哮喘共病的小鼠模型。然后使用该模型研究过敏性气道炎症对2009年甲型H1N1大流行性流感病毒感染小鼠肺部病理的影响。结果表明,在预先存在的甲型流感病毒感染中诱导急性过敏性气道炎症对肺部病理加重具有累加效应,这与人类流行病学研究结果相符。相比之下,预先存在的过敏性气道炎症可预防随后的甲型流感病毒感染,这与先前哮喘小鼠甲型流感病毒感染的小鼠模型结果一致。该小鼠模型的这些不同结果表明,过敏性气道炎症与甲型流感病毒感染之间的时间关系可能在哮喘和流感共病中起关键作用。因此,该小鼠模型将加深我们对甲型流感病毒感染如何影响哮喘宿主的理解,并可能有助于制定策略以改善对感染甲型流感病毒的哮喘患者的治疗和预后。