Mechanisms of cholinergic hyperfunction induced by IgE in human airways

在本研究中，我们在体外和体内研究了IgE对人气道胆碱能神经功能的影响。胆碱能收缩反应由电场刺激（EFS）或外源性乙酰胆碱（ACh）引起。与IgE孵育显着增强EFS诱导的支气管收缩和ACh释放与对照组织相比。自身受体M2功能也受到IgE孵育的损害。在体内研究中，36名过敏性鼻炎患者[17名具有低血清IgE（滴度为（SY）≤ 100%）]，其中10名患者具有低血清IgE（滴度为（SY）≤ 100%），10名患者具有低血清IgE（滴度为（SY）≤ 100%）。[250]、19例无下呼吸道疾病的高IgE（250<）患者和11例健康体检者。我们比较了他们对吸入抗胆碱能和β <@D22@>D2-肾上腺素能药物的支气管扩张反应。空气 ...更多信息 以1秒用力呼气量（FEV<@D21@>D2）评定气道口径。% FEVD 2值均大于80%，与血清IgE水平呈负相关（P<0.01）。在健康和过敏性鼻炎受试者中，次最大剂量的抗胆碱能药物引起小但显著的支气管扩张。血清IgE增高的变应性鼻炎患者FEV<@D21@>D2的增加明显更大（155 ± 1.05）。[）20 ml平均值（]SY. ±. [)SEM与健康对照组（64例）比较，差异有统计学意义（P<0.05）。[))21血清IgE水平低者（82 ± 0.01）%，过敏性鼻炎患者（82 ± 0.01）%。[))21 ml，P<0.05）。相比之下，β <@D22@>D2-肾上腺素能药物的作用在三组之间没有显著差异。我们得出结论，较高的血清IgE水平与较低的FEV<@D21@>D2值相关，抗胆碱能药物而非β <@D22@>D2-肾上腺素能药物导致高IgE受试者比低IgE过敏性鼻炎患者和健康受试者更明显的支气管扩张。这些体内数据表明，血清IgE可能是通过胆碱能机制决定气道口径的因素之一。少

In this study, we examined the effect of IgE on human airway cholinergic nerve function both in vitro and in vivo.In vitro study, human bronchi were obtained from 20 patients undergoing lung resection. Cholinergic contractile responses were induced by electrical field stimulation (EFS) or exogenous acetylcholine (ACh). Incubation with IgE significantly enhanced EFS-induced bronchial contraction and ACh release compared with those of control tissues. Autoreceptor M2 function was also impaired by IgE incubation. These in vitro results suggest that IgE itself can enhance cholinergic contraction via ACh release from the nerves possibly by M2 dysfunction.In vivo study, 36 allergic rhinitis patients [17 with low serum IgE (titer was (]SY.ltoreq.[) 250) and 19 with high serum IgE (250<) ] without lower respiratory tract diseases and 11 healthy subjects were enrolled in the study. We compared their bronchodilator responses to inhalation anti-cholinergic and beta<@D22@>D2-adrenergic agents. Air … More way caliber was assessed by forced expiratory volume in one second (FEV<@D21@>D2). %FEV<@D21@>D2 values of all patients were greater than 80% , but were negatively correlated with serum IgE levels (P<0.01). Submaximal doses of the anti-cholinergic agent caused small but significant bronchodilation in both healthy and allergic rhinitis subjects. The increase in FEV<@D21@>D2 was significantly greater in allergic rhinitis patients with high serum IgE(155 (]SY.+-。[)20ml mean(]SY.+-。[)SEM,P<0.05) than in healthy subjects (64(]SY.+-。[))21 ml) and those with allergic rhinitis but low serum IgE (82 (]SY.+-。[)) 21 ml, P<0.05). In contrast, the effects of the beta<@D22@>D2-adrenergic agent were not significantly different among the three groups. We concluded that higher serum IgE levels were correlated with lower FEV<@D21@>D2 values, and that the anti-cholinergic agent but not the beta<@D22@>D2-adrenergic agent causes more pronounced bronchodilation in high IgE subjects than in low IgE allergic rhinitis patients and healthy subjects. These in vivo data suggest that serum IgE may be one of the factors that determine the airway caliber via cholinergic mechanisms. Less