Hasegawa Shunji, Wakiguchi Hiroyuki, Okada Seigo, Gui Kang Yu, Fujii Nao, Hasegawa Masanari, Hasegawa Hideki, Ainai Akira, Atsuta Ryo, Shirabe Komei, Toda Shoichi, Wakabayashi-Takahara Midori, Morishima Tsuneo, Ichiyama Takashi
Department of Pediatrics, Yamaguchi University Graduate School of Medicine, 1-1-1 Minamikogushi, Ube, Yamaguchi 755-8505, Japan.
Department of Pediatrics, Yamaguchi University Graduate School of Medicine, 1-1-1 Minamikogushi, Ube, Yamaguchi 755-8505, Japan.
Cytokine. 2014 Oct;69(2):206-10. doi: 10.1016/j.cyto.2014.06.006. Epub 2014 Jul 6.
Several studies support the role of viral infections in the pathogenesis of asthma exacerbation. However, several pediatricians believe that influenza virus infection does not exacerbate bronchial asthma, except for influenza A H1N1 2009 pandemic [A(H1N1)pdm09] virus infection. We previously reported that A(H1N1)pdm09 infection possibly induces severe pulmonary inflammation or severe asthmatic attack in a mouse model of bronchial asthma and in asthmatic children. However, the ability of seasonal H1N1 influenza (H1N1) infection to exacerbate asthmatic attacks in bronchial asthma patients has not been previously reported, and the differences in the pathogenicity profiles, such as cytokine profiles, remains unclear in bronchial asthma patients after A(H1N1)pdm09 and H1N1 infections.
The cytokine levels and viral titers in the bronchoalveolar lavage (BAL) fluid from mice with and without asthma after H1N1 infection (A/Yamagata and A/Puerto Rico strains) were compared.
The interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-α, IL-5, interferon (IFN)-α, IFN-β, and IFN-γ levels were significantly higher in the BAL fluids from the control/H1N1 mice than from the asthmatic/H1N1 mice. The viral titers in the BAL fluid were also significantly higher in the control/H1N1mice than in the asthmatic/H1N1 mice infected with either A/Yamagata or A/Puerto Rico.
A(H1N1)pdm09 infection, but not H1N1 infection, can induce severe pulmonary inflammation through elevated cytokine levels in a mouse model of asthma.
多项研究支持病毒感染在哮喘加重发病机制中的作用。然而,一些儿科医生认为,除2009年甲型H1N1流感大流行病毒感染外,流感病毒感染不会加重支气管哮喘。我们之前报道过,甲型H1N1流感大流行病毒感染可能在支气管哮喘小鼠模型和哮喘儿童中诱发严重肺部炎症或严重哮喘发作。然而,季节性H1N1流感(H1N1)感染加重支气管哮喘患者哮喘发作的能力此前尚未见报道,而且在甲型H1N1流感大流行病毒和H1N1感染后的支气管哮喘患者中,细胞因子谱等致病性特征的差异仍不清楚。
比较H1N1感染(A/山形株和A/波多黎各株)后有哮喘和无哮喘小鼠支气管肺泡灌洗(BAL)液中的细胞因子水平和病毒滴度。
与哮喘/H1N1小鼠相比,对照/H1N1小鼠BAL液中的白细胞介素(IL)-6、IL-10、肿瘤坏死因子(TNF)-α、IL-5、干扰素(IFN)-α、IFN-β和IFN-γ水平显著更高。感染A/山形株或A/波多黎各株的对照/H1N1小鼠BAL液中的病毒滴度也显著高于哮喘/H1N1小鼠。
在哮喘小鼠模型中,甲型H1N1流感大流行病毒感染而非H1N1感染可通过升高细胞因子水平诱导严重肺部炎症。