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目的探讨诱导痰细胞和白细胞介素8(IL8)、白细胞介素9(IL9)、嗜酸性粒细胞趋化因子(eotaxin)在儿童哮喘发病中的作用及相互关系。方法以2004年9月至2005年3月重庆医科大学附属儿童医院确诊哮喘的44例患儿为研究对象,其中急性发作期25例、缓解期19例,同时选10例因骨骼畸形入院的患儿作对照组,进行诱导痰的细胞分类检查和ELISA方法检测IL8、IL9、eotaxin。结果哮喘患儿诱导痰细胞总数明显升高,急性发作期诱导痰中性粒细胞数明显高于缓解期和对照组,缓解期淋巴细胞数明显高于急性发作期和对照组,嗜酸性粒细胞各组间比较差异无显著性意义;哮喘患儿诱导痰IL8、IL9质量浓度与对照组比较有明显升高,且IL8、IL9质量浓度与中性粒细胞百分数呈正相关,eotaxin在各组间比较差异无显著性意义。结论与成人过敏性哮喘不同,中性粒细胞在儿童哮喘的发病中扮演重要角色,IL8趋化中性粒细胞聚集于气道,中性粒细胞在IL9的作用下产生和释放IL8,三者相互影响,共同参与哮喘的发病。
Objective To investigate the roles and relationships of induced sputum cells and interleukin 8 (IL8), interleukin 9 (IL9) and eotaxin in childhood asthma. Methods Forty-four children diagnosed with asthma at Chongqing Children’s Hospital Affiliated to Chongqing Medical University from September 2004 to March 2005 were studied. Among them, 25 cases were acute exacerbation, 19 cases were remission and 10 cases were admitted to hospital because of skeletal deformity Children as control group, the classification of induced sputum cells and ELISA detection of IL8, IL9, eotaxin. Results The total number of induced sputum cells in asthmatic children was significantly increased, the number of induced sputum neutrophils in acute episodes was significantly higher than that in remission and control groups, and the number of lymphocytes in remission was significantly higher than that in acute exacerbation and control group. Eosinophils There was no significant difference among the groups. The concentration of IL8 and IL9 induced sputum in children with asthma were significantly increased compared with the control group, and the concentrations of IL8 and IL9 were positively correlated with the percentage of neutrophils. The levels of eotaxin in each group were compared No significant difference between the significance. Conclusions Unlike adult allergic asthma, neutrophils play an important role in the pathogenesis of childhood asthma. IL8 chemotactic neutrophils accumulate in the airways and neutrophils produce and release IL8 under the action of IL9. Affect each other and jointly participate in the pathogenesis of asthma.