M2受体抗体在支气管哮喘发病中的实验性研究

目的测定Wistar大鼠外周血中M2受体的自身抗体，观察地塞米松对M2受体的自身抗体影响以及M2受体的自身抗体在哮喘发病中的可能机制。方法以卵白蛋白致敏制备Wistax大鼠哮喘模型，分为健康对照组、哮喘模型组和地塞米松组。以细胞外第二环表位肽段的合成肽作为抗原，分别通过SA—ELISA检测各组大鼠外周血中的M2受体的自身抗体，计算抗体阳性率和抗体滴度的几何均数；观察各组动物哮喘发作症状、末次卵白蛋白致敏攻击24h内支气管肺泡灌洗液中嗜酸性粒细胞的数量及支气管肺组织病理学改变。结果哮喘模型组的M2受体自身抗体阳性率为66．7％，明显高于对照组的8．3％和地塞米松组的16．7％（P〈0．05）；哮喘模型组自身抗体阳性患者的抗体滴度为1-105，明显高于对照组的1—20和地塞米松组的1-30（P〈0．05）。在哮喘模型组中，M2受体的自身抗体阳性率和抗体滴度明显高于健康对照组与地塞米松组，地塞米松组的BALF中的嗜酸性粒细胞与哮喘组相比有明显减少，地塞米松组的气道炎症程度轻于哮喘组。结论应用地塞米松可以降低M2受体的自身抗体阳性率和抗体滴度，提示M2受体的自身抗体可能参与哮喘的病理生理过程。

Experimental study on the role of antibodies against M2-muscarinic acetylcholine receptor in the pathogenesis of asthma

Objective To investigate whether autoantibody against M2-muscarinic acetylcholine receptor is related to asthma and the effect of dexamethasone on this autoantibody. Methods Thirty-six Wistar healthy rats were divided randomly into three experimental groups: normal control group, asthmatic model group and dexamethasone treatment group, and asthmatic models were established by ovalbumin. The synthetic peptide M2-muscarinic acetylcholine receptor which corresponds to amino acids sequences of the second extracellular loop of human was used as antigens to detect serum autoantibody against M2-muscarinic acetylcholine receptor from three groups by SA-ELISA. Symptoms of asthmatic attack, airway inflammation and inflammatory cells in BALF were observed in three groups. Results The positive rate of autoantibody against M2-muscarinic acetylcholine receptor in asthmatic model group was 66.7% which was significantly higher than that of dexamethasone treatment group(16.7%) and normal control group(8.3%, P < 0.05). Anti-M2-receptor antibody titers in asthmatic model group and dexamethasone treatment group were 1:105 and 1:30, respectively. Conclusion The rate of positive antibody and the titers of antibody against M2-muscarinic acetylcholine receptor were significant higher in asthmatic model group than in dexamethasone treatment group and normal control group. Eosinophils in BALF were lower in dexamethasone treatment group than in asthmatic model group. It suggests that antibody against M2-muscarinic acetylcholine receptor plays a very important role in the pathophysiology of asthma.