哮喘鼠白细胞介素23水平变化及其作用机制

目的：通过检测哮喘鼠血清白细胞介素23（IL-23）在激素治疗前后的水平变化及与IL-4、IFN-γ、IL-17的相关性，探讨其在哮喘发病中的作用。方法：将30只健康雌性BALB/C小鼠按完全随机设计原则分为3组，每组10只，即OVA致敏并激发的哮喘模型组（A 组）、鸡卵白蛋白(OVA)致敏、激发并予激素治疗组（B组）和正常对照组（C 组）。末次激发24 h后，各组小鼠摘眼球取血，ELISA法检测血清IgE、IL-4、IFN-γ、IL-17和IL-23的含量。结果：① 小鼠的行为学改变、血清IgE水平增高以及 IL-4 显著增高而 IFN-γ降低、IL-4与IFN-γ呈负相关等，均证明哮喘模型制备成功。② A组小鼠血清中IL-23 的水平 ［(155.56±12.50) ng·L^-1］ 高于C组［(51.49±6.34) ng·L^-1］，而B组小鼠血清IL-23 的水平 ［(88.00±6.43) ng·L^-1］ 低于A组（P＜0.01）。③ IL-23与IL-17含量成正相关关系(r= 0.763，P＜0.05)，与IL-4、IFN-γ均无相关性。结论：IL-23参与哮喘的发病，糖皮质激素对其有抑制作用。IL-23可能是通过诱导IL-17的产生间接促进哮喘发病，IL-23对于Th1 类细胞因子IFN-γ及 Th2 类细胞因子IL-4均无明显调节作用。

Change of interleukin-23 level in mouse asthma model and its action mechanism

Objective To measure the change of serum interleukin-23(IL-23) level before and after treatment with glucocortcoid and analyze the correlations between levels of IL-23 and IL-4,IFN-γ,IL-17,and explore the role of IL-23 in bronchial asthma.Methods Thirty femal BALB/c mice were randomly divided into three group(n=10): group A(asthma model),group B(corticosteroid treatment) and group C(normal control).All mice were killed 24 h after final OVA challenge.The blood samples were obtained for measurements of serum IgE,IL4,IFN-γ,IL-17and IL-23 levels by enzyme-linked immunoabsorbent assay(ELISA).Results The mouse asthma model appeared ethological changes specific to asthma.The level of OVA specific IgE in serum increased.The level of serum IL-4 increased and the level of IFN-γ decreased.Correlation analysis showed negative relationship between IL-4 and IFN-γ(r=-0.859,P<0.01),there existed Th1/Th2 imbalance.The level of serum IL-23 in group A was higher than that in group C(P<0.01).In mice treated with inhaled budesonide(group B),the level of serum IL-23 was lower than that in group A(P<0.01).The concentration of IL-23 had no correlation with both IL-4 and IFN-γ.There was a positive correlation between the levels of serum IL-23 and IL-17(r=0.763,P<0.01).Conclusion IL23 in serum might be involved in the pathogenesis of bronchial asthma,and could be inhibited by inhaled glucocorticoid.IL-23 has no relationship with IFN-γ and IL-4.It suggested that IL-23 might contribute to the development of asthma indirectly by inducing IL-17 generation.