Division of Pulmonary and Critical Care Medicine, Oregon Health and Science University, Portland, Oregon, USA.
J Leukoc Biol. 2018 Jul;104(1):61-67. doi: 10.1002/JLB.3MR1117-426R. Epub 2018 Apr 6.
Airway eosinophils are increased in asthma and are especially abundant around airway nerves. Nerves control bronchoconstiction and in asthma, airway hyperreactivity (where airways contract excessively to inhaled stimuli) develops when eosinophils alter both parasympathetic and sensory nerve function. Eosinophils release major basic protein, which is an antagonist of inhibitory M muscarinic receptors on parasympathetic nerves. Loss of M receptor inhibition potentiates parasympathetic nerve-mediated bronchoconstriction. Eosinophils also increase sensory nerve responsiveness by lowering neurons' activation threshold, stimulating nerve growth, and altering neuropeptide expression. Since sensory nerves activate parasympathetic nerves via a central neuronal reflex, eosinophils' effects on both sensory and parasympathetic nerves potentiate bronchoconstriction. This review explores recent insights into mechanisms and effects of eosinophil and airway nerve interactions in asthma.
气道中的嗜酸性粒细胞在哮喘中增多，并且特别丰富于气道神经周围。神经控制支气管收缩，在哮喘中，当嗜酸性粒细胞改变副交感神经和感觉神经功能时，气道高反应性（气道对吸入的刺激过度收缩）就会发展。嗜酸性粒细胞释放主要碱性蛋白，它是副交感神经上抑制性 M 毒蕈碱受体的拮抗剂。M 受体抑制的丧失增强了副交感神经介导的支气管收缩。嗜酸性粒细胞还通过降低神经元的激活阈值、刺激神经生长和改变神经肽表达来增加感觉神经的反应性。由于感觉神经通过中枢神经元反射激活副交感神经，因此嗜酸性粒细胞对感觉神经和副交感神经的影响增强了支气管收缩。这篇综述探讨了哮喘中嗜酸性粒细胞与气道神经相互作用的机制和影响的最新见解。
