The mechanism of development and exacerbation of virus-induced asthma analyzed by a lipid mediator gene knock-out mice

为了阐明病毒感染导致哮喘加重的发病机制，我们使用呼吸道合胞病毒（RSV）感染的实验性哮喘模型小鼠，检测了支气管阻力、外周血和支气管肺泡液（BALF）分析以及多种类型的细胞因子/趋化因子。与对照组相比，卵清蛋白（OVA）和OVA/RSV组BALF和组织嗜酸性粒细胞水平显著升高。BALF中MIP-1α在OVA/RSV组较RSV组、OVA组和对照组显著升高。OVA组血清IL-5和OVA/RSV组血清IL-17也高于对照组。提示MIP-1α介导的嗜酸性粒细胞炎症反应可能在呼吸道合胞病毒诱导的哮喘急性加重过程中起重要作用。

To clarify the pathogenesis of exacerbations of asthma due to viral infection, we examined bronchial resistance, peripheral blood and bronchial alveolar fluid (BALF) analyses and multiple types of cytokines/chemokines using an experimental asthma model mice infected with respiratory syncytial virus (RSV). The levels of BALF and tissue eosinophils showed significant increase in ovalbumin (OVA) and OVA/RSV groups compared with controls. MIP-1αin BALF was significantly increased in OVA/RSV groups compared with RSV groups, OVA groups, and control groups. Serum IL-5 in OVA groups and serum IL-17 in OVA/RSV groups were also higher than in controls. These findings suggest that eosinophilic inflammation via MIP-1α may play an important role in acute exacerbations of asthma model induced by RSV.