哮喘联盟

   摘要
   背景：几项研究支持病毒感染在哮喘发作的发病机制中有作用。然而，一些儿科医生认为，除了2009年大流行的甲型H1N1流感[A型（H1N1）pdm09]病毒感染，流感病毒感染未加重支气管哮喘。我们曾报道：A（H1N1）pdm09感染可能引起严重的肺部炎症或在支气管哮喘小鼠模型和哮喘患儿中引发重度哮喘发作。然而，季节性甲型H1N1流感（甲型H1N1）感染加重支气管哮喘患者哮喘发作的能力尚未被报道，他们致病性情况的差异，如支气管哮喘患者在感染A型（H1N1）pdm09和H1N1后的细胞因子水平目前还不清楚。
   方法：试验比较了哮喘和没有哮喘小鼠经H1N1感染（A/山县和A/波多黎各株）后的支气管肺泡灌洗（BAL）液中的细胞因子水平和病毒量。
   结果：对照/H1N1流感小鼠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的水平较哮喘/H1N1小鼠显著升高。对照/H1N1流感小鼠BAL液中的病毒水平较感染A/山县或A/波多黎各的哮喘/H1N1小鼠显著升高。
   结论：甲型（H1N1）pdm09感染，而非H1N1感染，可以通过提高哮喘小鼠模型的细胞因子水平引发严重的肺部炎症。
 

（苏楠 审校）
Cytokine. 2014 Jul 3;69(2):206-210. doi: 10.1016/j.cyto.2014.06.006. [Epub ahead of print]

 

Cytokine profile of bronchoalveolar lavage fluid from a mouse model of bronchial asthma during seasonal H1N1 infection.
 

Hasegawa S1, Wakiguchi H2, Okada S2, Gui Kang Y2, Fujii N2, Hasegawa M2, Hasegawa H3, Ainai A4, Atsuta R5, Shirabe K6, Toda S6, Wakabayashi-Takahara M2, Morishima T7, Ichiyama T2.
 

ABSTRACT
BACKGROUND: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: A(H1N1)pdm09 infection, but not H1N1 infection, can induce severe pulmonary inflammation through elevated cytokine levels in a mouse model of asthma.
 

Cytokine. 2014 Jul 3;69(2):206-210. doi: 10.1016/j.cyto.2014.06.006. [Epub ahead of print]