Objective To investigate the effect of tobacco smoke exposure on airway inflammatory cell infiltration and the expression of nuclear transcription factor-κB p65 (NF-κB p65) in lung tissues of bronchial asthma mice.
Methods Forty female BALB/c mice (SPF grade) were randomly divided into 4 groups, including normal control group, asthma group, tobacco smoke exposure group, tobacco smoke exposure + asthma group, with 10 mice in each group. The replication of bronchial asthma mice model was sensitized by aerosol inhalation of OVA, while the normal control group was sensitized by aerosol inhalation of normal saline. The tobacco smoke exposure group was exposed to cigarette smoke for 1 hour after each atomization. Bronchoalveolar lavage fluid (BALF) was collected after 28 days, and blood cells (WBC), eosinophils (EOS) and neutrophils (NEU) in BALF were determined. The protein expression levels of NF-κB p65 were detected by Western-blot.
Results The total number of leukocytes, acidophilic granulocyte, neutrophilsin BALF in the asthma and tobacco smoke exposure +asthma group were significantly higher than the control group and tobacco smoke exposure group, the total number of leukocytes and neutrophil count in BALF in the tobacco smoke exposure+asthma group were significantly higher than those of the asthma group, while eosinophils count were significantly lower than that in the asthma group ( P<0.05). NF-κB p65 protein expression was increased in the lung tissues of the asthma group and tobacco smoke exposure + asthma group, and the increase was more obvious in the tobacco smoke exposure + asthma group ( P<0.05). There was a linear positive correlation between white blood cell count and NF-κB p65 expression level in the lung tissues of the tobacco smoke exposure + asthma group ( r= 0.781, P=0.008).
Conclusion Tobacco smoke exposure may promote airway inflammatory cell infiltration in bronchial asthma by up-regulating the expression of NF-κB p65 protein.
摘要： 目的 探讨烟草烟雾暴露对支气管哮喘小鼠气道炎性细胞浸润及肺组织核转录因子-κB p65 (NF-κB p65) 表达的影响。 方法 将雌性无特定病原体级 (specific pathogen free, SPF) 级BALB/c纯系小白鼠40只随机分为4组, 即 正常对照组、哮喘组、烟草烟雾暴露组和烟草烟雾暴露+哮喘组, 每组各10只。正常对照组给予雾化吸入生理盐水, 哮 喘组给予雾化吸入卵蛋白 (OVA) 致敏从而复制模型, 烟草烟雾暴露组则在正常对照组基础上予以烟草烟雾暴露1 h, 而 烟草烟雾暴露+哮喘模型组则在哮喘模型组的基础上给予同样的烟草烟雾暴露1 h。28 d后采集支气管肺泡灌洗液 (BALF), 测定BALF中白细胞(WBC)、嗜酸性粒细胞 (EOS) 及中性粒细胞 (NEU)计数。用蛋白质免疫印迹法 (Westernblot) 检测肺组织NF-κB p65蛋白表达水平。 结果哮喘组、烟草烟雾暴露+哮喘组小鼠BALF中白细胞总数、嗜酸粒细 胞、中性粒细胞均高于对照组及烟草烟雾暴露组, 烟草烟雾暴露+哮喘组BALF中白细胞总数和中性粒细胞计数高于哮 喘组, 嗜酸粒细胞计数低于哮喘组 ( P<0.05); 哮喘组、烟草烟雾暴露+哮喘组小鼠肺组织NF-κB p65蛋白表达均上升, 但 烟草烟雾暴露+哮喘组小鼠升高更明显, 与哮喘组相比差异有统计学意义 ( P<0.05)。烟草烟雾暴露+哮喘组白细胞计数 与肺组织NF-κB p65表达水平呈正相关 ( r=0.781, P=0.008) 。 结论烟草烟雾暴露可能通过上调NF-κB p65蛋白表达, 促进支气管哮喘气道炎性细胞浸润。