Influenza virus-induced lung inflammation was modulated by cigarette smoke exposure in mice.
Influenza virus-induced lung inflammation was modulated by cigarette smoke exposure in mice.
复制标题
小鼠香烟烟雾暴露可调节流感病毒引起的肺部炎症
DOI：
10.1371/journal.pone.0086166
复制
发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Lau YL
中科院分区：
文献类型：
--
作者：
Han Y;Ling MT;Mao H;Zheng J;Liu M;Lam KT;Liu Y;Tu W;Lau YL
虽然吸烟者对季节性流感病毒感染的易感性和严重性增加，但目前还没有关于吸烟者感染2009年大流行H1N1（pdmH 1 N1）或禽流感H9 N2（H9 N2/G1）病毒风险的报告。在我们的研究中，我们使用小鼠模型来研究香烟烟雾对pdmH 1 N1或H9 N2病毒感染的影响。小鼠暴露于香烟烟雾21天，然后感染pdmH 1 N1或H9 N2病毒。对照组小鼠平行暴露于空气中。我们发现，香烟烟雾暴露单独显着上调肺部炎症。这种先前的香烟烟雾暴露显著降低了随后的pdmH 1 N1或H9 N2病毒感染的疾病严重程度。对于pdmH 1 N1感染，香烟烟雾暴露小鼠的死亡率显著低于对照小鼠，这可能是由于炎性细胞因子和趋化因子的产生显著减少。类似地，在H9 N2感染后，香烟烟雾暴露的小鼠显示出显著更少的体重减轻，这可能归因于与对照小鼠相比更低的细胞因子和趋化因子产生，更少的巨噬细胞、中性粒细胞、CD 4+和CD 8 + T细胞浸润以及减少的肺损伤。为了进一步研究潜在的机制，我们使用尼古丁在体外和体内模拟香烟烟雾的作用。用尼古丁预处理原代人巨噬细胞72 h显著降低了pdmH 1 N1或H9 N2感染后细胞因子和趋化因子的表达。在pdmH 1 N1或H9 N2感染后，皮下和连续给予尼古丁的小鼠显示出比对照小鼠显著更少的体重减轻和更低的炎症反应。此外，α7烟碱乙酰胆碱受体敲除小鼠在香烟烟雾暴露和H9 N2感染后体重减轻比野生型小鼠更多。我们的研究提供了第一个证据表明，在香烟烟雾暴露的小鼠中，pdmH 1 N1和H9 N2病毒的致病性被减轻，这可能部分归因于尼古丁的免疫抑制作用。
Although smokers have increased susceptibility and severity of seasonal influenza virus infection, there is no report about the risk of 2009 pandemic H1N1 (pdmH1N1) or avian H9N2 (H9N2/G1) virus infection in smokers. In our study, we used mouse model to investigate the effect of cigarette smoke on pdmH1N1 or H9N2 virus infection. Mice were exposed to cigarette smoke for 21 days and then infected with pdmH1N1 or H9N2 virus. Control mice were exposed to air in parallel. We found that cigarette smoke exposure alone significantly upregulated the lung inflammation. Such prior cigarette smoke exposure significantly reduced the disease severity of subsequent pdmH1N1 or H9N2 virus infection. For pdmH1N1 infection, cigarette smoke exposed mice had significantly lower mortality than the control mice, possibly due to the significantly decreased production of inflammatory cytokines and chemokines. Similarly, after H9N2 infection, cigarette smoke exposed mice displayed significantly less weight loss, which might be attributed to lower cytokines and chemokines production, less macrophages, neutrophils, CD4+ and CD8+ T cells infiltration and reduced lung damage compared to the control mice. To further investigate the underlying mechanism, we used nicotine to mimic the effect of cigarette smoke both in vitro and in vivo. Pre-treating the primary human macrophages with nicotine for 72 h significantly decreased their expression of cytokines and chemokines after pdmH1N1 or H9N2 infection. The mice subcutaneously and continuously treated with nicotine displayed significantly less weight loss and lower inflammatory response than the control mice upon pdmH1N1 or H9N2 infection. Moreover, α7 nicotinic acetylcholine receptor knockout mice had more body weight loss than wild-type mice after cigarette smoke exposure and H9N2 infection. Our study provided the first evidence that the pathogenicity of both pdmH1N1 and H9N2 viruses was alleviated in cigarette smoke exposed mice, which might partially be attributed to the immunosuppressive effect of nicotine.
登录
查看更多内容
影响因子：
6.7
作者：
Goodman AG;Fornek JL;Medigeshi GR;Perrone LA;Peng X;Dyer MD;Proll SC;Knoblaugh SE;Carter VS;Korth MJ;Nelson JA;Tumpey TM;Katze MG
通讯作者：
Katze MG
影响因子：
4.4
作者：
Chen, Haiyan;Cowan, Mark J.;Medvedev, Andrei E.
通讯作者：
Medvedev, Andrei E.
影响因子：
168.9
作者：
Brusselle, Guy G.;Joos, Guy F.;Bracke, Ken R.
通讯作者：
Bracke, Ken R.
影响因子：
9.4
作者：
Butt, KM;Smith, GJD;Guan, Y
通讯作者：
Guan, Y
DOI：
10.1165/rcmb.2009-0254oc
发表时间：
2010-09-01
影响因子：
6.4
作者：
Jaspers, Ilona;Horvath, Katherine M.;Noah, Terry L.
通讯作者：
Noah, Terry L.