室内空气污染物诱发哮喘的分子机理

近十年来随着现代免疫学，分子生物学的迅速发展，对哮喘有了许多新的认识，并提出了许多新观点，哮喘成为分子生物学和医学研究的新热点，新观点之一认为：气道神经源性炎症是哮喘发作的一个重要原因。长期以来，许多学者怀疑空气污染物对哮喘发作协同作用，但是空气污染物是如何引起哮喘发作的分子机理并不清楚。1991年丹麦学者Nielsen GD首先提出一种新的假说，认为气道刺激作用是一种受体介导的病理学过程，包含了“空气污染物／辣椒素受体／Ca^2 /P物质／速激肽受体”信息传递分子链，气道神经源性炎症正是这一过程在气道局部的反映，由于缺乏实验证实，这项假说成为悬案，1997年美国学者Caterina MJ研究组成功地克隆了感觉神经纤维末梢上辣椒素受体，为验证这一假说提供了坚实的物质基础。

Molecular Mechanism of Asthma Induced by Indoor Air Pollutants

During the last decade a lot of new learning about asthma was arisen along with the development of modern immunology and molecular biology,and asthma had been one hotspot in the studies of molecular biological and administer medical field.One of the new viewpoints was that airway neurogenic inflammation took important role in asthma development.For years scholars had suspected that airborne pollutants had an synergistic effect on the attack of asthma and could cause asthma attack,but they did not know the molecular mechanism.In 1991 Denish scholar Nielsen GD advanced a new hypothesis that airway irritation was mediated by capsaicin receptor.The pathological process included a molecular chain of message transfer as air pollutants_capsaicin receptor_Ca2+_substance P_neurokinin receptor.Airway neurogenic inflammation was the result of activation of the receptors.In 1997 American scholar Caterina MJ and his colleagues successfully obtained the cloned capsaicin receptor in expressing cells,this will make Nielsen GD's hypothesis living.