被动吸烟增加幼鼠日后发展为哮喘的气道炎症

Cigarette smoke exposure of immature mice increase asthmatic airway inflammation in adult mice

目的:在整体水平探索幼鼠被动吸烟对日后哮喘形成后气道炎症反应的影响。方法:幼鼠被动吸烟3周,进入成年后建立OVA致敏的BALB/c小鼠哮喘模型。40只BALB/c小鼠随机分为4组:生理盐水/空气组、生理盐水/被动吸烟组、OVA/空气组和OVA/被动吸烟组,每组10只。通过HE染色检测小鼠肺组织病理变化,细胞计数检测肺泡灌洗液中细胞(嗜酸性粒细胞、中性粒细胞、淋巴细胞、巨噬细胞)数目,ELISA方法检测肺泡灌洗液中细胞因子(IL-4、IL-5、IL-13)和血清中OVA-IgE、OVA-IgG1、OVA-IgG2a的表达情况,并检测各组小鼠的气道反应性。结果:幼年时期被动吸烟暴露可显著增加小鼠成年后OVA致敏哮喘模型的气道高反应性,血清OVA-IgE、OVA-IgG1、OVA-IgG2a表达,气道炎性细胞浸润和炎性细胞因子分泌(P<0.05)。结论:幼年期被动吸烟可显著增加OVA致敏成年小鼠的气道炎症和气道高反应性,这可能为哮喘的防治提供新思路。

Objective：To investigate the influence of cigarette smoke （CS） exposure on immature mice which were established as asthma model in the adult. Methods ： Immature mice exposed to cigarette smoke for three weeks, after entering aduhhood, OVA- sensitized asthma model was established. Forty mice were randomly allocated into four groups： normal saline （NS）/air group, NS/CS group, OVA/air group, and OVA/CS group, ten mice in each group. The pathological changes of the lung tissue were determined by HE staining, the numbers of macrophages, eosinophils, lymphocytes, neutrophils in bronchoalveolar lavage fluid （BALF） were counted, the cytokines IFN-γ,IL-4 ,IL-5, IL-13 in BALF and the serum OVA-IgE, OVA-IgG1, OVA-IgG2a levels were detected by ELISA, and the airway responsiveness was measured by body plethysmograph. Results： Immature mice exposed to cigarette smoke can increase airway responsiveness, up-regulated serum OVA-IgE, OVA-IgG1, OVA-IgG2a levels, exacerbated the airway inflammatory cells infiltration and cytokines secretion in asthmatic mice induced by OVA in adult mice compare to OVA/air group （P〈0. 05 ）. Conclusion： Cigarette smoke exposure in immature mice can significantly increase airway inflammation and airway responsiveness in OVA-sensitized adult mice,which may provide new ideas for the treatment of asthma.