目的 通过建立小鼠哮喘模型,观察小鼠肺组织IL-17和IL-6表达以及地塞米松对其的影响.方法 选择雄性Balb/c小鼠30只,随机分为正常对照组、哮喘模型组和地塞米松治疗组,每组各10只.采用ELISA和免疫组织化学标记法分别测定和标记肺部IL-6和IL-17.结果 苏木精-伊红染色显示哮喘模型组肺标本有明显非特异性炎症反应征象.哮喘模型激发同时给予地塞米松治疗后,肺匀浆IL-6和IL-17水平均下降(P ＜ 0.05).模型组肺组织免疫组化标记显示IL-17显著表达于小支气管柱状上皮细胞.IL-6免疫组化标记结果同IL-17,但表达较IL-17低.结论 Th17细胞参与了哮喘的发病机制,地塞米松对IL-17和IL-6有抑制作用.%Objective To investigate the expressions of IL-6 and IL-17 m lung tissue of asthmatic mice model and dexamethasone on the impact of the above factors. Methods 30 male Balb/c mice were randomly divided into three groups: the normal control group (group A), the asthmatic model group (group B) and the dexamethasone treated group (group C). Mice were sensitized and challenged with ovalbumin (OVA) to establish asthma models,and groups C were treated with dexamethasone (2 mg/kg, 7 d). The expressions of IL-17 and IL-6 in lung tissue were detected by ELISA and immunohistochemistry. In order to understand lymphocytic infiltration in lung tissue, CD3,CD20 and CD79 in each group were also dectected by immunohistochemistry. Airway inflammation in lung tissue was observed by HE staining. Results In asthmatic model group, the levels of IL-6 and IL-17 increased compared with the dexamethasone group (P ＜ 0.05), and the expression of IL-17 increased significantly on small bronchial columnar epithelial cells by immunohistochemistry. After treatment, the expression of IL-17 was decreased in dexamethasone group. The results of IL-6 in each group were similar to those of IL-17 by immunohistochemistry, but the signal was lower than IL-17. Lymphocytic infiltration was observed for T lymphocytes (CD3+) and B lymphocytes (CD20+ CD79+)under bronchial mucosa. Inflammation was evident in the lung tissue of asthma model by HE staining. Conclusions Thl7
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