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哮喘气道炎症中嗜酸性粒细胞凋亡与IL—5、IL—10关系的研究
引用本文:刘春涛,雷松,等.哮喘气道炎症中嗜酸性粒细胞凋亡与IL—5、IL—10关系的研究[J].华西医科大学学报,2001,32(1):55-58.
作者姓名:刘春涛  雷松
作者单位:[1]华西医科大学附属第一医院呼吸内科,成都610041 [2]附属第一医院肿瘤治疗中心
摘    要:目的 动态观察哮喘动物模型气道嗜酸性细胞凋亡在炎症中的意义和调控机理。研究IL-5和IL-10对凋亡的调节作用。方法 卵白蛋白(OVA)腹腔注射与雾化吸入诱发BALB/c小鼠哮喘发作,在激发后0、8、24、48、96小时及7、14天行BAL,ELISA法测定IL-5、IL-10浓度。CD15、CD49d双色标记嗜酸细胞(EOS),流式细胞仪上检测EOS凋亡率。结果 OVA激发后电镜观察显示肺内有明显炎性细胞浸润和细胞凋亡。哮喘组EOS凋亡水平与对照大体相似,EOS凋亡率与IL-10/IL-5比值密切相关。结论 IL-5和IL-10分别上行和下行调节哮喘气道炎症。气道局部有EOS凋亡现象,并受到IL-5、IL-10相互作用的调节。

关 键 词:哮喘  嗜酸性粒细胞  细胞因子  细胞凋亡  IL-5  IL-10

A kinetic study on the relationship between of IL-5, IL-10 and eosinophil apoptosis in asthmatic airway inflammation]
C Liu,Z Wang,Y Feng,S Lei.A kinetic study on the relationship between of IL-5, IL-10 and eosinophil apoptosis in asthmatic airway inflammation][J].Journal of West China University of Medical Sciences,2001,32(1):55-58.
Authors:C Liu  Z Wang  Y Feng  S Lei
Institution:Department of Respirology, First Affiliated Hospital, WCUMS, Chengdu 610041, China.
Abstract:OBJECTIVE: To observe time-course profile of eosinophil apoptosis, in murine asthma models in airway explicate its implication for asthmatic inflammation remission, and investigate the role of IL-5 and IL-10 in modulating cell apoptosis. METHODS: An animal model of asthma was established by OVA sensitizing-challenging BALB/c mice. Histologic study of lung tissue was made with the use of electronmicroscope. At seven points (0 h, 8 h, 24 h, 48 h, 96 h, Day 7 and Day 14) in the time course after challenge, bronchoalveolar lavage (BAL) was performed obtain BAL cells and recover fluid. Levels of IL-5 and IL-10 were detected by ELISA. Cell apoptosis was assayed by PI stain on a flow cytometer. RESULTS: After challenge, apoptosis of eosinophils, lymphocytes, endothelial cells could be seen under the electronmicroscope. IL-5 in BALF elevated significantly whereas no significant difference was found between the levels of IL-10 in BALF before and after challenge. Eosinophil apoptosis was identified and a two-phase elevation of apoptosis percentages was observed, although no significant difference was found between average apoptosis in asthmatic group and that in control. Data analyses revealed a negative correlation between apoptosis percentages and the levels of IL-5, and a closer correlation between the percentages and IL-5/IL-10 ratio. CONCLUSION: IL-5 and IL-10 could up- and down-regulate asthmatic airway inflammation, respectively. EOS underwent apoptosis in situ and this was modulated by IL-5 and IL-10 interaction.
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