论文部分内容阅读
目的 建立粉尘螨变应原经皮致敏、滴鼻激发诱发的“特应性皮炎-哮喘”小鼠模型.方法 以C57 BL/6J小鼠为研究对象,通过反复破坏皮肤屏障后贴敷粉尘螨变应原经皮致敏、然后给予粉尘螨滴鼻激发气道炎症的方法制备特应性皮炎-哮喘小鼠模型,并从皮肤及肺组织病理、免疫炎症分子定量表达、支气管肺泡灌洗液中炎症细胞计数以及气道高反应性检测等不同方面对小鼠模型进行评估.结果 模型小鼠致敏处皮肤组织病理呈典型的湿疹样改变,皮损中Th2型细胞因子表达显著升高,Th1型细胞因子表达与对照差异无统计学意义.模型小鼠支气管肺泡灌洗液中细胞总数显著增多,其中淋巴细胞和嗜酸细胞数量显著高于对照组.肺组织病理可见支气管周围明显的嗜酸性粒细胞为主的炎症细胞浸润,肺组织中Th2型细胞因子表达也显著升高.模型小鼠经气道吸入甲酰胆碱后肺阻力随甲酰胆碱浓度升高而显著增加,肺动态顺应性则显著下降.结论 成功建立粉尘螨变应原经皮致敏诱导的“特应性皮炎-哮喘”动物模型,为特应性进程发病机制的研究提供了方法.“,”Objective To establish a mouse model of atopic march induced by epicutaneous sensitization and nasal challenge with dust mite allergen.Methods C57BL/6J mice were subjected to repeated epicutaneous sensitization with dust mite allergen or saline and then challenged with intranasal administration of mite allergen to induce airway inflammation.The mouse model was evaluated in terms of pathology of skin and lung,quantitative mRNA expression of inflammatory molecules,count of inflammatory cells in bronchoalveolar lavage fluid,and airway hyperresponsiveness.Results Mite allergen sensitized mice exhibited typical pathological changes of eczematous dermatitis and significantly higher expression levels of Th2 cytokines in lesions while Thl cytokines remained unchanged in comparison with normal controls.The number of total cells,lymphocytes and eosinophils in the bronchial alveolar lavage fluid were significantly higher in model mice than in the controls.Pulmonary histopathology showed peribronchial infiltration of eosinophils.The expression levels of Th2 cytokine mRNA in lung tissue also significantly increased.Methacholine dose-dependently induced increase in the lung resistance and decrease in the dynamic compliance of the lungs in mouse model.Conclusion In this study,we use epicutaneous sensitization and nasal challenge to successfully establish the mite allergen induced atopic march model.