Leech S C, Price J F, Holmes B J, Kemeny D M
Department of Child Health, Guy's, King's and St Thomas' School of Medicine, London, UK.
Allergy. 2000 Jan;55(1):74-8. doi: 10.1034/j.1398-9995.2000.00222.x.
Viruses cause asthmatic exacerbations in schoolchildren. We tested the hypothesis that children who wheezed with viral respiratory tract infections secrete higher levels of the type 1 cytokine interferon-gamma (IFN-gamma) in the peripheral circulation than children who had never wheezed. Blood was taken from 13 children (eight atopic) with episodic wheeze and 11 controls. CD4 and CD8 cells were separated from peripheral blood mononuclear cells and stimulated with phorbol 12-myrisate 13-acetate (PMA) and ionomycin for 24 h. IFN-gamma, IL-4, and IL-5 were measured in the supernatant by ELISA. IFN-gamma production by CD4 and CD8 cells was lower in children with a history of wheeze (CD4, P = 0.046; CD8, P = 0.037). These children were then analysed according to atopic status. CD4 and CD8 IFN-gamma production in nonatopic wheezy children was reduced (CD4, P=0.009; CD8, P=0.003). IFN-gamma production by atopic wheezy children was lower than by controls, but the differences were not significant (CD4, P = 0.2831; CD8, P = 0.1372). CD8 IL-5 was lower in children who wheezed (P=0.012). Release of IL-4 and IL-5 by CD4 cells did not differ between the three groups. We propose that defective IFN-gamma secretion by CD4 and CD8 cells may contribute to viral-induced wheeze in nonatopic children.
病毒可引发学龄儿童哮喘急性发作。我们检验了这样一个假设：与从未喘息过的儿童相比，因病毒性呼吸道感染而喘息的儿童外周循环中1型细胞因子干扰素-γ（IFN-γ）的分泌水平更高。采集了13名发作性喘息儿童（8名特应性儿童）和11名对照儿童的血液。从外周血单个核细胞中分离出CD4和CD8细胞，并用佛波酯12-肉豆蔻酸酯13-乙酸酯（PMA）和离子霉素刺激24小时。通过酶联免疫吸附测定法（ELISA）测量上清液中的IFN-γ、白细胞介素-4（IL-4）和白细胞介素-5（IL-5）。有喘息病史的儿童中，CD4和CD8细胞产生的IFN-γ较低（CD4，P = 0.046；CD8，P = 0.037）。然后根据特应性状态对这些儿童进行分析。非特应性喘息儿童的CD4和CD8 IFN-γ产生减少（CD4，P = 0.009；CD8，P = 0.003）。特应性喘息儿童的IFN-γ产生低于对照组，但差异不显著（CD4，P = 0.2831；CD8，P = 0.1372）。喘息儿童的CD8 IL-5较低（P = 0.012）。三组之间CD4细胞释放的IL-4和IL-5没有差异。我们提出，CD4和CD8细胞分泌IFN-γ存在缺陷可能导致非特应性儿童出现病毒诱导的喘息。
