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DEVELOPMENT OF DIAGNOSIS AND TREATMENT BASED ON PATHOPHYSIOLOGY OF CHRONIC COUGH

基于慢性咳嗽病理生理学的诊断和治疗进展

基本信息

批准号：
14570546
负责人：
FUJIMURA Masaki
金额：
$ 2.18万
依托单位：
KANAZAWA UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2002
资助国家：
日本
起止时间：
2002 至 2004
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14570546/
关键词：
chronic cough atopic cough cough variant asthma pressure stress to airway cough sensitivity airway smooth muscle contraction outcome ニューロペプチド原因アレルゲン長期予後

项目摘要

I. Basic research1. guinea pig models for atopic cough and cough variant asthma have been developed.1) Using the atopic cough model, it has been disclosure d that increased level of substance P resulted from antigen-induced inactivation of neutral endopeptidase is important in the antigen-induced increase in cough sensitivity, and that there may bean interaction between histamine and substance P.2) Using the cough variant asthma model, It is clarified that cough is elicited via antigen-induced bronchoconstridion, and that leukotrienes, but not tachykinins, are involved in the cough.2. We developed a apparatus to give quantitative mechanical pressure stress to guinea pig airway. The Mechanical pressure stress to airway induced cough reflex hypersensitivity associated with airway neutrophilic inflammation., suggesting self-perpetuating cycle between cough and cough hypersensitivity.II. Clinical research1. In addition to the difference of pathophysiologic feature between atopic cough and cough variant astluna, we elucidated the long-term outcome is also different between these two condition.: Nearly 30% patients with cough variant asthma develops typical asthma within several years but no patient with atopic cough does.2. Bronchial hyperresponsiveness and no use of long-tern inhaled corticosteroids were risk factors of typical asthma onset from cough variant asthma.3. Our prospective study confirmed that cough variant asthma, atopic cough and sinobronchial syndrome are common causes of chronic cough in Japan.

一、基础研究1．已开发出特应性咳嗽和咳嗽变异性哮喘的豚鼠模型。 1) 使用特应性咳嗽模型，已揭示抗原诱导的中性肽链内切酶失活导致的 P 物质水平增加对于抗原诱导的咳嗽敏感性增加很重要，并且组胺和 P 物质之间可能存在相互作用。 2) 使用咳嗽变异性哮喘模型，阐明了咳嗽是通过抗原诱导的支气管收缩引起的，咳嗽涉及白三烯，但速激肽不参与。2．我们开发了一种向豚鼠气道施加定量机械压力的装置。气道机械压力应激诱发与气道中性粒细胞炎症相关的咳嗽反射超敏反应，提示咳嗽和咳嗽超敏反应之间存在自我延续的循环。临床研究1.除了特应性咳嗽和咳嗽变异性哮喘之间病理生理学特征的差异外，我们还阐明了这两种情况之间的长期结局也不同：近30%的咳嗽变异性哮喘患者在几年内发展为典型哮喘，但特应性咳嗽患者没有这样做。 2．支气管高反应性和长期不使用吸入性糖皮质激素是咳嗽变异性哮喘典型发作的危险因素。 3．我们的前瞻性研究证实，咳嗽变异性哮喘、特应性咳嗽和窦支气管综合征是日本慢性咳嗽的常见原因。