柯萨奇B3病毒感染致小鼠气道上皮细胞粘附分子和MHCⅡ类分子高表达

Effect of CVB_3 infection on expression of adhesive molecules and MHCⅡ on the epithelia of mice trachea

目的:观察小鼠雾化吸入柯萨奇B3病毒(CVB3)后气道上皮细胞粘附分子ICAM-1、VCAM-1及MHCⅡ类分子表达的变化,初步探讨CVB3感染对机体免疫系统的影响及其在气道慢性炎症和哮喘发病机制中的作用。方法:将C57BL/6N小鼠随机分为4组:生理盐水组(NS)、生理盐水+卵蛋白组(NS+O)、病毒感染组(V)、病毒感染+卵蛋白组(V+O)。采用ELISA法测定血清CVB3抗体;取肺组织作常规病理制片,HE染色;甲苯胺蓝改良染色法镜下显示肥大细胞。提取气道上皮细胞采用流式细胞仪分析ICAM-1、VCAM-1及MHCⅡ类分子的表达。结果:病毒组小鼠血清中CVB3-IgM的OD值明显高于非病毒组(P<0.01)。病理检查肺组织可见:病毒组肺间质有较多炎细胞浸润,尤其肥大细胞浸润明显。V组、V+O组气道上皮细胞ICAM-1、VCAM-1和MHCⅡ类分子的表达明显增高,与NS组、NS+O组相比差异非常显著(P<0.01);V+O组增高更加显著,与V组比较也有显著差异(P<0.01);并可持续至少1个月。结论:小鼠雾化吸入CVB3后可致气道慢性炎症及粘附分子ICAM-1、VCAM-1和MHCⅡ类分子显著的高表达;在CVB3所致的气道炎症期间再接触过敏原两者对炎症免疫反应有协同作用。CVB感染后的炎症免疫反应在哮喘发病机制中起着非常关键的作用。

Objective：To study the effect of CVB3 infection on expression of adhesion molecule and MHCⅡmolecule on the epithelia of trachea and its roles in pathogenesis of chronic airway inflammation,airway hyperreactivity and asthma.Methods：C57 BL/6N mice were designated randomly in four groups：CVB3 infection group（V）and CVB3 infection with ovalbumin sensitization group（V＋O）,normal saline（NS）and normal saline with ovalbumin sensitization（NS＋O）.At the indicated time,specific IgM to CVB3 in serum was detected by ELISA method,and the lung were prepared for routine histological evaluation.Epithelium of trachea was isolated after digestion to examine the expression of ICAM-1,VCAM-1 and MHCⅡon the epithelium by flow cytometry.Results：CVB3 group had a higher CVB3 specific IgM in serum than that of non-CVB3 group and the difference were significant.Histological evaluation showed that more inflammatory cells especially mast cells were infiltrated in CVB3 group.ICAM-1,VCAM-1 and MHCⅡ expression in the epithelial cells increased significantly in CVB3 group when compared with non-CBV3 group（P〈0.01）.Importantly,expression of ICAM-1,VCAM-1and MHCⅡ increased much more significantly in the group of virus infection and ovalbumin sensitization group than that of virus infection alone（P〈0.01）and the higher expression could last for one month.Conclusion：CVB3 infection may upregulate the expression of ICAM-1 VCAM-1and MHCⅡon the airway epithelial cells and this perhaps contributes to persistent airway hyperreactivity.Adhesion molecules play important roles in the pathogenesis for asthma caused by virus infection.