Fukuyama Satoshi, Shoemaker Jason E, Zhao Dongming, Nagajima Noriko, Tomita Yuriko, Maemura Tadashi, da Silva Lopes Tiago Jose, Watanabe Tokiko, Yamayoshi Seiya, Hasegawa Hideki, Kawaoka Yoshihiro
Division of Virology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan.
Department of Chemical and Petroleum Engineering, Swanson School of Engineering, University of Pittsburgh, Pittsburgh, PA, USA.
Npj Viruses. 2024 Mar 25;2(1):16. doi: 10.1038/s44298-024-00026-4.
Influenza A(H7N9) virus showed high pathogenicity in humans when it emerged in 2013. Cigarette smoke (CS) causes pulmonary diseases including bronchitis, emphysema, and lung cancer. Although habitual smoking is thought to increase the risk of severe seasonal influenza virus infection, its effect on A(H7N9) virus infection is poorly understood. Here, we employed a mouse model of long-term exposure to CS to investigate the effect of CS on the pathogenicity of A(H7N9) virus infection. Unexpectedly, body weight loss for mice exposed to CS was milder than that for mock-treated mice upon A(H7N9) virus infection. CS exposure improved the survival rate of A(H7N9) virus-infected mice even though virus titers and pathological changes in the lungs were not significantly different between CS-exposed and control mice. Microarray analysis showed that CS-exposure activates cytokine/chemokine activity, immune response, and cell cycle activities that resemble reactivities against A(H7N9) virus infection. Therefore, under conditions where cytokine and chemokine expression in the lungs is already high due to CS exposure, the enhanced expression of cytokines and chemokines caused by A(H7N9) virus infection might be less harmful to the organs compared to the rapid increase in cytokine and chemokine expression in the air-exposed mice due to the infection. CS may thus induce immunoregulatory effects that attenuate severe pulmonary disease during A(H7N9) virus infection. However, these findings do not support CS exposure due to its many other proven negative health effects.
甲型H7N9流感病毒在2013年出现时对人类具有高致病性。香烟烟雾（CS）会引发包括支气管炎、肺气肿和肺癌在内的肺部疾病。尽管习惯性吸烟被认为会增加严重季节性流感病毒感染的风险，但其对甲型H7N9流感病毒感染的影响却知之甚少。在此，我们采用长期暴露于香烟烟雾的小鼠模型来研究香烟烟雾对甲型H7N9流感病毒感染致病性的影响。出乎意料的是，在感染甲型H7N9流感病毒后，暴露于香烟烟雾的小鼠体重减轻程度比假处理小鼠要轻。尽管暴露于香烟烟雾的小鼠和对照小鼠的病毒滴度及肺部病理变化并无显著差异，但香烟烟雾暴露提高了感染甲型H7N9流感病毒小鼠的存活率。微阵列分析表明，香烟烟雾暴露激活了细胞因子/趋化因子活性、免疫反应以及类似于针对甲型H7N9流感病毒感染的反应的细胞周期活性。因此，在因香烟烟雾暴露导致肺部细胞因子和趋化因子表达已经很高的情况下，与因感染导致空气暴露小鼠体内细胞因子和趋化因子表达迅速增加相比，甲型H7N9流感病毒感染引起的细胞因子和趋化因子表达增强对器官的危害可能较小。因此，香烟烟雾可能会诱导免疫调节作用，从而减轻甲型H7N9流感病毒感染期间的严重肺部疾病。然而，由于香烟烟雾还有许多其他已被证实的负面健康影响，这些发现并不支持接触香烟烟雾。
