Gleich G J, Jacoby D B, Fryer A D
Department of Immunology, Mayo Clinic, Rochester, MN 55905, USA.
Int Arch Allergy Immunol. 1995 May-Jun;107(1-3):205-7. doi: 10.1159/000236978.
Evidence exists that eosinophil cationic proteins damage respiratory epithelium in bronchial asthma. Furthermore, the degree of eosinophilia in the blood and the lung is related to bronchial hyperreactivity. The eosinophil might increase airway irritability by increasing vagal responsiveness. Sensitized challenged guinea pigs develop M2 muscarinic receptor cholinergic dysfunction which is abolished by injection of heparin or polyglutamate and both the eosinophil granule major basic protein and the eosinophil peroxidase act as allosteric M2 receptor antagonists. Thus, eosinophil-associated pulmonary inflammation in asthma may enhance vagally mediated bronchoconstriction.
有证据表明，嗜酸性粒细胞阳离子蛋白会损害支气管哮喘患者的呼吸道上皮。此外，血液和肺部嗜酸性粒细胞增多的程度与支气管高反应性有关。嗜酸性粒细胞可能通过增加迷走神经反应性来提高气道易激性。致敏激发的豚鼠会出现M2毒蕈碱受体胆碱能功能障碍，注射肝素或聚谷氨酸可消除这种障碍，嗜酸性粒细胞颗粒主要碱性蛋白和嗜酸性粒细胞过氧化物酶均作为变构M2受体拮抗剂发挥作用。因此，哮喘中与嗜酸性粒细胞相关的肺部炎症可能会增强迷走神经介导的支气管收缩。
