Mechanisms of cholinergic hyperfunction induced by IgE in human airways
IgE诱导人呼吸道胆碱能亢进的机制
基本信息
- 批准号:08670644
- 负责人:
- 金额:$ 1.41万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:1996
- 资助国家:日本
- 起止时间:1996 至 1997
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
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
在这项研究中,我们检查了IgE对人类气道胆碱能神经功能的影响。在体外和体内,从20例接受肺切除术的患者中获得了人支气管。通过电场刺激(EFS)或外源性乙酰胆碱(ACH)诱导胆碱能收缩反应。与对照组织相比,与IGE的孵育显着增强了EFS诱导的支气管收缩和ACH释放。自身受体M2功能也因IgE孵育而受损。这些体外结果表明,IgE本身可以通过M2功能障碍从神经中释放出ACH来增强胆碱能的收缩。在体内研究中,36例过敏性鼻炎患者[17个低血清IgE(Sy.ltoreq。[] 250)和19对高血清IgE(250 <)进行了研究(250 <)的研究(250 <),而没有静止疗法疗法和11个健康的诊断。我们比较了他们对吸入抗胆碱能和β<@d22@> d2-肾上腺素能剂的支气管扩张剂反应。空气…通过一秒钟内强制到期量评估口径的更多方式(FEV <@d21@> d2)。 %FEV <@d21@> D2的所有患者值大于80%,但与血清IgE水平负相关(p <0.01)。在健康和过敏性鼻炎受试者中,抗胆碱能剂的次最大剂量引起了小但显着的支气管扩张。在过敏性鼻炎患者中,FEV <@d21@> D2的增加明显更大(155(]SY。+ - 。[)20ml平均值(]SY。+ - 。[)SEM,p <0.05),比健康受试者(64(64(SY.+ - 。] 21 mL)和SY+Serum serum serum Ige(82)。 ML,P <0.05)。相反,在这三组中,β<@d22@> d2-肾上腺素的效果没有显着差异。我们得出的结论是,较高的血清IgE水平与较低的FEV <@d21@> d2值相关,而抗胆碱能剂,而不是β<@d22@> d2-d2-d2-d2-adrenrenagic剂会导致高IGE受试者比低IGE Antergic Altergic Altergic Ryinitis患者和健康的受试者和健康的健康受试者和健康的健康受试者。这些体内数据表明,血清IgE可能是通过胆碱能机制确定气道口径的因素之一。较少的
项目成果
期刊论文数量(24)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Miura M: "Impairment of neural nitric oxide-mediated relaxation after antigen exposure in guinea pig airways in vitro." Am J Respir Crit Care Med. 156. 217-222 (1997)
Miura M:“豚鼠气道体外抗原暴露后神经一氧化氮介导的松弛受损。”
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- 影响因子:0
- 作者:
- 通讯作者:
Ohuchi Y: "The Induction of nitric oxide synthase by LPS inhalation enhances substance P-induced microvascular leakage." Eur Respir J. (in press).
Ohuchi Y:“吸入 LPS 诱导一氧化氮合酶可增强 P 物质诱导的微血管渗漏。”
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- 影响因子:0
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Ichinoue, M: "A neurokinin l-receptor antagonist improves exercise-induced airway narrowing in asthma patients." Am J Respir Crit Care Med. 153. 936-941 (1996)
Ichinoue, M:“神经激肽 l 受体拮抗剂可改善哮喘患者运动引起的气道狭窄。”
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- 影响因子:0
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Ichinose M: "Incubation with IgE increases cholinergic neurotransmission in human airways in vitro." Am. J. Respir. Crit. Care Med.154. (1996)
Ichinose M:“在体外,与 IgE 一起孵育可增加人体气道中的胆碱能神经传递。”
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- 影响因子:0
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Ichinose M: "A neurokinin 1-receptor antagonist improves exercise-induced airway narrowing in asthmatic patients." Am. J. Respir. Crit. Care Med.153. 936-941 (1996)
Ichinose M:“神经激肽 1 受体拮抗剂可改善哮喘患者运动引起的气道狭窄。”
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ICHINOSE Masakazu其他文献
ICHINOSE Masakazu的其他文献
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{{ truncateString('ICHINOSE Masakazu', 18)}}的其他基金
Modulation of Inflammatory Process in COPD Airways
慢性阻塞性肺病气道炎症过程的调节
- 批准号:
12470132 - 财政年份:2000
- 资助金额:
$ 1.41万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Mechanisms of airway injury by peroxynitrite
过氧亚硝酸盐损伤气道的机制
- 批准号:
10470148 - 财政年份:1998
- 资助金额:
$ 1.41万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Study of airway neurogenic inflammation in chronic animal model and the evidence of axon reflex mechanisms in human airways
慢性动物模型气道神经源性炎症研究及人类气道轴突反射机制的证据
- 批准号:
04670455 - 财政年份:1993
- 资助金额:
$ 1.41万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)