Effects of allergic airway disease on mouse adenovirus type 1 respiratory infection
Effects of allergic airway disease on mouse adenovirus type 1 respiratory infection
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DOI：
10.1016/j.virol.2009.06.009
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发表时间：
2009-08-15
期刊：
影响因子：
3.7
通讯作者：
Weinberg, Jason B.
中科院分区：
文献类型：
--
作者：
Anderson, Victoria E.;Nguyen, Y. N.;Weinberg, Jason B.
病毒感染可能参与哮喘的发病机制。反过来，Th 2极化的肺部环境可能会增加宿主对感染的易感性。我们使用蟑螂抗原（CRA）过敏性气道疾病模型来检验Th 2细胞因子过度产生增加对小鼠腺病毒1型（MAV-1）易感性的假设。CRA致敏导致IL-4和IL-13的肺表达上调、肺细胞炎症和过度的气道粘液产生。鼻内MAV-1感染后，在感染后7天，CRA致敏小鼠的肺细胞炎症比未致敏小鼠更明显，但在随后的时间点则没有。CRA致敏没有显著抑制肺IFN-γ表达，并且在MAV-1感染过程中，CRA致敏小鼠和未致敏小鼠的肺IFN-γ表达均上调。尽管CRA诱导的肺部炎症的差异，MAV-1在肺和脾中的生命负荷和MAV-1在肺中的基因表达没有显着差异，在CRA致敏和未致敏小鼠。因此，我们的数据表明，MAV-1的发病机制是不直接或间接的Th 2极化与过敏性气道疾病。(C)2009 Elsevier Inc. All rights reserved.
Virus infection may contribute to asthma pathogenesis. In turn, a Th2-polarized pulmonary environment may increase host susceptibility to infection. We used a cockroach antigen (CRA) model of allergic airway disease to test the hypothesis that Th2 cytokine overproduction increases Susceptibility to mouse adenovirus type 1 (MAV-1). CRA sensitization led to upregulated lung expression of IL-4 and IL-13, lung cellular inflammation, and exaggerated airway Mucus production. Following intranasal MAV-1 infection, lung cellular inflammation was more pronounced in CRA-sensitized mice than in unsensitized mice at 7 days post-infection but not at a later time point. CRA sensitization did not significantly Suppress lung IFN-gamma expression, and lung IFN-gamma expression was upregulated in both CRA-sensitized mice and unsensitized mice over the Course of MAV-1 infection. Despite CRA-induced differences in pulmonary inflammation, MAV-1 vital loads in lung and spleen and MAV-1 gene expression in the lung did not differ between CRA-sensitized and unsensitized mice. Our data therefore Suggest that MAV-1 pathogenesis is not affected directly or indirectly by the Th2 polarization associated with allergic airway disease. (C) 2009 Elsevier Inc. All rights reserved.