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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。
Plasma and peripheral blood mononuclear cells (PBMCs) from 28 asthmatic children were tested for IL-10 production by PHA stimulation and NO and IL-2 levels were measured by double-antibody sandwich ELISA. Results: ① The levels of IL-10 in plasma and PBMC of children with acute asthma after PHA stimulation were significantly lower than those of normal children (P <0.01), and both of them were still lower than normal in the remission of asthma (P0.05); ②The level of NO in children with acute exacerbation was significantly higher (P0.05), and returned to normal in remission The levels of IL-2 produced by PBMC in PHA-stimulated group were significantly increased (P <0.01), but returned to normal in remission stage (P> 0.05). ④Acute exacerbation of asthma in PBMC produced IL-10 There was a significant negative correlation between IL-2 and IL-2 (r = -0.504, P <0.01), but not with plasma NO level (r = -0.319, P> 0.05). Tip: IL-10 secretion and release of asthma attack reduced, elevated levels of NO and IL-2, causing or aggravating chronic airway inflammation, causing airway hyperresponsiveness induced or exacerbated asthma.