摘要
目的:探讨巨噬细胞炎性蛋白—1α(MIP-1α),正常T细胞活化后所表达和分泌
的调节蛋白(regulated upon activation normal T cell expressed and secreted,RANTES)
在呼吸道合胞病毒(Respiratory syncytial virus,RSV)感染发病机制中的作用,并
探讨这些趋化因子的表达与呼吸道高气道反应的相关性。
方法:收集45例RSV感染患儿的血清,其中10例支气管哮喘,15例支气管炎
或肺炎,20例上呼吸道感染;20例无RSV感染的健康婴儿,用ELISA法测定其血
清MIP-1α,RANTES的水平。
结果:RSV感染患儿的血清MIP-1α,RANTES的水平明显高于健康婴儿(P<0.05
或P<0.01);支气管哮喘组和支气管炎或肺炎组患儿的血清MIP-1α,RANTES的水
平明显高于上呼吸道感染组;支气管哮喘组与支气管炎或肺炎组患儿血清MIP-1α,
RANTES的水平无显著性差异;另外,血清MIP-1α,RANTES的水平与血液中嗜酸
性粒细胞数密切相关。
结论:RSV感染后血清趋化因子MIP-1α,RANTES表达增加,导致患儿气道嗜
酸性粒细胞聚集,产生炎症,并产生气道高反应,可能是RSV感染致哮喘的病理基
石出。
Objective: To explore the roles of macrophage inflammatory protein-1alpha (MIP-1α) and regulated upon activation normal T cell expressed and secreted(RANTES) in the pathogenesis of respiratory syncytial virus(RSV) infection, and to explore the correlation of the concentrations of MIP-1α and RANTES in serum and airway hyperresponsiveness,Methods: Serum samples were obtained from 45 infants with RSV infection, including 10 bronchial asthma , 15 bronchiolitics or pneunonia , 20 upper respiratory tract infection ; 20 healthy infants with non- RSV infection as the normal group. ELISA method was used to determine the concentrations of MIP-1α and RANTES in serum.ResultS: MIP-1α and RANTES levels in infants with RSV infection were much higher than those of non- RSV infected healthy subjects (P<0.05 or P<0.01). MIP-1α and RANTES levels of bronchial asthma and those of severe RSV infection subjects were much higher than upper respiratory tract infection subjects. But these was no significant different between bronchial asthma and those of severe RSV infection group. It was also found that serum concentrations of MIP-1α and RANTES were positively correlated to the number of eosinophilis.Conclusions: The concentrations of chemokines of MIP-1α and RANTES in serum will increase after respiratory syncytial virus infection, leading to eosinophilis recruiting, lung inflammatory and airway hyperresponsiveness, which may be the pathological base for RSV infection to bronchitis asthma .
引文
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