摘要
采用双抗夹心ELISA技术检测了28例哮喘患儿血浆及外周血单个核细胞(PBMC)在植物血凝素(PHA)刺激下产生IL-10水平,同时检测了NO和IL-2水平。结果:①急性发作期哮喘患儿血浆及PBMC在PHA刺激下产生IL-10水平均比正常儿童显著降低(P<0.01),在哮喘缓解期虽均有所恢复,但仍低于正常儿童(P<0.05);②NO水平在急性发作期患儿明显升高(P<0.05),而在缓解期恢复正常(P>0.05);③急性发作期哮喘患儿在PHA刺激下PBMC产生IL-2水平明显升高(P<0.01),但在缓解期恢复正常(P>0.05);④急性发作期哮喘患儿在PHA刺激下PBMC产生IL-10水平与IL-2呈显著负相关(r=-0.504,P<0.01),而与血浆NO水平相关不显著(r=-0.319,P>0.05)。提示:哮喘发作时IL-10分泌及释放减少,NO和IL-2水平升高,导致或加重气道慢性炎症反应,引起气道高反应性而诱发或加重哮喘。
We used double antibody sandwich ELISA for the quantitative determination of plasma IL10 level and the production of IL2, 10 by PHAactivated peripheral blood mononuclear cells (PBMC) level in 28 asthmatic children and 20 matched normal children. At the same time, the plasma nitrite and nitrate(NO2/NO3) level was determined. Results showed that asthmatic children in acute attack stage(pretherapy) had decreased amounts of the plasma IL10 and the production of IL10 by PHAactivated PBMC compared with normal control subjects (7.21±2.22,11.16±2.88;22.16±5.58,64.11±10.44pg/ml, respectively, both of the P<0.01), while in restoration stage (posttherapy) which had restored in some degree, but still lower than the normal levels(9.25±1.62,56.84±10.43,respectively, P<0.05). Asthmatic children in acute attack stage had increased amounts of the plasma NO2/NO3 and the production of IL2 by PHAactivated PBMC compared with normal control subjects (NO2/NO3:32.67±4.51,29.64±2.93μmol/L;IL2:21357±5978,16152±3411cpm, respectively, P<0.05,0.01 respectively),while in restoration stage which had decreased amounts of the plasma NO2/NO-3 and the production of IL2 by PHAactivated PBMC to normal levels (NO2/NO3:30.18±3.09μmol/L;17068±3514cpm,respectively, both of the P>0.05). Linear correlation analysis showed obvious correlation between the production of IL10 and IL2 by PHAactivated PBMC. The results suggest that there was decreased release and secretion of IL10, and increased production of IL2 and NO in asthmatic children, which could cause or increase airway hyperresponsiveness in some degree. They might play important roles in immunological mechanisms of asthma.
出处
《免疫学杂志》
CAS
CSCD
北大核心
1998年第3期179-181,共3页
Immunological Journal
基金
第三军医大学大坪医院基金