Kingham P J, Costello Richard W, McLean W Graham
Department of Pharmacology, University of Liverpool, Liverpool, UK.
Pulm Pharmacol Ther. 2003;16(1):9-13. doi: 10.1016/S1094-5539(02)00093-7.
In vivo, eosinophils localise to airway nerves in patients with asthma as well as in animal models of hyperreactivity. In both, in vivo and in vitro studies, we have shown that this localisation changes both cholinergic nerve and eosinophil function. In particular, it leads to an increase in acetylcholine release due to loss of function of a neuronal autoreceptor, the M(2) muscarinic receptor. This loss of M(2) receptor function occurs because eosinophils become activated and degranulate as a result of interactions that occur via specific adhesion molecules expressed on nerves that are recognised by counter ligands on eosinophils.
在体内,嗜酸性粒细胞定位于哮喘患者以及高反应性动物模型的气道神经中。在体内和体外研究中,我们均已表明这种定位改变了胆碱能神经和嗜酸性粒细胞的功能。特别是,由于神经元自身受体M2毒蕈碱受体功能丧失,它导致乙酰胆碱释放增加。M2受体功能丧失的发生是因为嗜酸性粒细胞因通过神经上表达的特定粘附分子与嗜酸性粒细胞上的反配体发生相互作用而被激活并脱颗粒。