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Th2细胞因子和粘附分子在变应性鼻炎和变应性哮喘发病机制中的作用
The roles of Th2 cytokines and adhesion molecular in the pathogenesis of allergic rhinitis and allergic asthma
【摘要】 目的探讨白细胞介素13(interleukin13,IL-13)、白细胞介素5(interleukin-5,IL-5)和血管细胞粘附分子-1(vascular cellular adhesion mo-lecular-1,VCAM-1)在上下呼吸道变应性炎症一致性中的作用。方法采用6-8周雄性SD大鼠,随机分成变应性鼻炎组10只,鼻炎对照组10只,哮喘组10只和哮喘对照组10只,以卵清蛋白致敏激发制成变应性鼻炎和变应性哮喘模型。HE染色和甲苯胺蓝染色分别检测变应性鼻炎模型鼻粘膜和哮喘模型鼻粘膜及肺组织中嗜酸粒细胞、肥大细胞,免疫组化检测上述组织中IL13、IL-5和VCAM-1的表达。结果变应性鼻炎模型鼻粘膜和变应性哮喘模型肺组织中嗜酸粒细胞、肥大细胞数、VCAM-1和IL-13阳性血管数以及IL-13和IL-5阳性炎症细胞数明显多于相应对照组。结论Th2细胞因子和粘附分子的表达是变应性鼻炎和变应性哮喘共同的机制。
【Abstract】 OBJECTIVE To evaluate the roles of interleukin-1 3 (IL-1 3), interlevkin-5(IL-5) and vascular cellular adhesion molecular-1 (VCAM-1 ) in the pathogenesis of allergic rhinitis and asthma, METHODS Forty rats were randomly divided into four groups, which were allergic rhinitis group (AR group), control of AR (con AR), asthma group (AS group), and control of AS (con AS). The allergic rhinitis and asthma were made by injecting egg white protein, The infiltration of eosinophils and mast cells were detected by hematotoxylin-eosin staining (HE staining) and toluidine blue staining respectively, The expressions of IL-1 3, IL-5 and VCAM-1 in nasal mucosa and lung tissue were examined by immunohistochemical stainings. RESULTS The numbers of eosinophils and mast cells in nasal mucosa of AR group were significantly higher than those in nasal mucosa of con AR, and also significantly higher in AS than in Con AS, The same results happened in the numbers of VCAM-1 and IL-1 3 positive vessels, the numbers of IL-1 3 and IL-5 positive inflammatory cells in both nasal and lung tissues, were significantly higher in AR and AS groups than in their controls, CONCLUSION Th2 cytokines and VCAM-1 may play important roles in the pathogenesis of allergic rhinitis and allergic asthma.
【Key words】 Rhinitis, Allergic, Perennial; Asthma; Interleukin-5; Interleukin-1 3; Vascular Cell Adhesion Molecule -1;
- 【文献出处】 中国耳鼻咽喉头颈外科 ,Chinese Archives of Otolaryngology-head and Neck Surgery , 编辑部邮箱 ,2004年01期
- 【分类号】R765;R562.25
- 【被引频次】12
- 【下载频次】425