中文摘要：

目的：应用卵清蛋白（OVA）建立大鼠变应性鼻炎（AR）模型,探讨Toll样受体（TLR）2和4亚型（TLR2和TLR4）在AR发病中调节非特异性免疫和特异性免疫的作用。方法：80只大鼠随机分为正常组、AR模型组、AR＋脂多糖（LPS）组和AR＋肽聚糖（PGN）组,每组20只。HE染色观察各组大鼠鼻黏膜组织形态学改变并计数炎症细胞浸润数,免疫组织化学法检测各组大鼠鼻黏膜组织中TLR2、TLR4和IgE蛋白表达水平,Real-time PCR法检测各组大鼠鼻黏膜组织中TLR2和TLR4mRNA表达水平。结果：与正常组比较,模型组、AR＋LPS组和AR＋PGN组大鼠鼻部症状评分和炎症细胞计数明显升高（P〈0.05）。与正常组比较,模型组大鼠鼻黏膜组织变应性损伤明显,鼻黏膜以嗜酸性粒细胞浸润为主,AR＋LPS组和AR＋PGN组大鼠鼻黏膜组织以中性粒细胞浸润为主。与正常组比较,模型组、AR＋LPS组和AR＋PGN组大鼠鼻黏膜组织中TLR2、TLR4和IgE表达水平明显增高（P〈0.05）;与模型组比较,AR＋LPS组大鼠鼻黏膜组织中TLR4和IgE表达水平明显升高（P〈0.05）;AR＋PGN组大鼠鼻粘膜组织中TLR2和IgE的表达水平较模型组也明显升高（P〈0.05）。结论：应用OVA腹腔注射及局部喷鼻能有效建立AR模型,TLR2和TLR4在AR发病中发挥调节非特异性免疫与特异性免疫的作用。

英文摘要：

Objective To build the rat allergic rhinitis（AR）model with OVA,and to investigate the role of TLR subunits 2and 4in the pathogenesis of AR in rats.Methods 80 rats were randomly divided into normal group,model group,AR＋LPS group and AR＋PGN group（n=20）.The morphological changes of nasal mucosa tissue and the number of inflammatory cells and infiltration were observed by HE staining.The expression levels of TLR2,TLR4 and IgE in nasal mucosa tissue were measured with immunohistochemical method.Real time-PCR was used to evaluate the expression levels of TLR2 mRNA and TLR4 mRNA in the nasal mucosa tissue of the rats in various groups.Results Compared with normal control group,the scores of nasal symptoms and the number of inflammatory cells in model group,AR＋LPS group and AR＋PGN group were significantly increased（P〈0.05）.Compared with normal group,the allergic injury of nasal mucosa of the rats in model group was obvious;the eosinophil count and the expression levels of TLR2,TLR4 and IgE in model group were significantly increased（P〈0.05）,while the neutrophil count was significantly increased in LPS group（P〈0.05）.Compared with model group,the expression levels of TLR4 and IgE in AR＋LPS group were significantly increased（P〈0.05）,and the expression levels of TLR2 and IgE in AR ＋ PGN group were significantly increased（P〈0.05）.Conclusion Intraperitoneal injection and local nasal of OVA could effectively build AR model;TLR2and TLR4 play an important role in the pathogenesis of AR.