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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有协同作用 ,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NielsenGD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/Ca2 +/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CaterinaMJ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
With the rapid development of modern immunology and molecular biology in the past decade, there are many new understandings of asthma and many new ideas have been proposed. Asthma has become a new hot spot in molecular biology and medical research. One of the new ideas is that airway neurogenic inflammation is an important cause of asthma attacks. For a long time, many scholars suspect that air pollutants have a synergistic effect on asthma attacks. However, the molecular mechanism of how air pollutants cause asthma attacks is not clear. In 1991, the Danish scholar NielsenGD first proposed a new hypothesis that airway stimulation is a receptor-mediated pathological process that includes “air pollutants / capsaicin receptor / Ca2 + / substance P / Peptide receptor ”information transmission molecular chain, airway neurogenic inflammation is the reflection of this process in the airways. Due to lack of experiments, this hypothesis became a pending case. In 1997, the American scholar Caterina MJ successfully cloned the capsaicin receptor on the sensory nerve fibers and provided a solid material basis for the verification of this hypothesis