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目的 :探讨白细胞介素 -10 (以下简称IL -10 )与过敏性哮喘发病的关系。方法 :对 5 0例过敏性哮喘患者以及 5 0例正常对照者外周血单个核细胞 (以下简称PBMC)分别在有无过敏原以及糖皮质激素存在的条件下 ,体外培养后采用双抗体夹心酶联免疫吸附法 ,分别测定上清IL -10分泌水平。结果 :过敏性哮喘PBMC培养后自发分泌IL -10水平显著低于正常对照组 (P <0 0 1) ,加入屋尘螨 (HDM 10 μg/ml)培养条件下 ,过敏性哮喘PBMC分泌IL -10更低 ,与同组自发管有显著差异 (P <0 0 1)。两者在地塞米松 ( 10 μg/ml)培养条件下 ,PBMC分泌IL -10均较各同组自发管增加 ,差异有显著性。 (P <0 0 0 5 ) ,但过敏性哮喘增加幅度明显高于正常对照。结论 :过敏性哮喘发病时 ,体内T细胞受抗原刺激影响合成分泌IL -10减少 ,使IL -10对哮喘的免疫抑制能力下降 ,与哮喘发病有关。糖皮质激素促进T淋巴细胞分泌IL -10可能是糖皮质激素抗炎作用的机理之一。
Objective: To investigate the relationship between interleukin-10 (IL-10) and the development of allergic asthma. Methods: Peripheral blood mononuclear cells (PBMCs) from 50 allergic asthmatic patients and 50 normal controls were cultured in vitro with or without allergen and glucocorticoid respectively. The level of IL-10 secreted by the supernatant was measured by ELISA. Results: The levels of IL - 10 secreted spontaneously in allergic asthma PBMC were significantly lower than those in normal control group (P <0.01) 10 was lower, with significant differences with the spontaneous management of the same group (P <0.01). Both dexamethasone (10 μg / ml) culture conditions, PBMC secretion of IL-10 compared with the same group spontaneous increase, the difference was significant. (P <0 0 05), but the increase rate of allergic asthma was significantly higher than that of the normal control. CONCLUSIONS: In the pathogenesis of allergic asthma, T cells in the body are affected by antigen stimulation to reduce the synthesis and secretion of IL-10, and to decrease the immunosuppressive capacity of IL-10 on asthma, which is related to the pathogenesis of asthma. Glucocorticoids promote the secretion of IL-10 by T lymphocytes may be one of the mechanisms of the anti-inflammatory effect of glucocorticoids.