臭氧在诱发过敏性哮喘中的作用及其分子机制

It has been a serious public health problem that the morbidity of Asthma is increasing over whole world. The increase of the non-allergen air pollutant has a close relationship to the increasing morbidity of Asthma and the theory of atopy stressor explains this phenomenon commendably. With the quick development of the urban, the Ozone pollution has been an outstanding global air pollution problem. As a kind of non-allergen air pollutant, Ozone has exactly causal relationship with the occurrence and development of the Asthma, but its molecular mechanisms are still unclear. So this item puts forward that Ozone is a kind of atopy stressor , it can action as the transient receptor potential vanilloid subtype 1（TRPV1）'s gamete , and activated the TRPV1 signal transmission system which starts with the mast cells ,and makes the Ca2+ flow into the cytes causing the mast cells release IL-4,promoting the B lymphocytes to produce a large number of IgE and resulting in the founding of acquired atopy, with the effect of the allergen , causing Allergic Asthma. Methods This item will carry out with the whole animal experiment and vitro cell experiment to research the Ozone's effect of atopy stressor and through the TRPV1 signal transmission system which starts with the mast cells inducing allergic asthma, using CPZ blocking-up this signal transmission system and reveal the molecular mechanisms of Ozone inducing allergic asthma by analyzing Ca2+、IL-4、IgE and the end effect of Asthma . And provide theory basis for the future to recognize the crowd who are sensitive to the Ozone and strengthen the asthma prevention and control measures.

哮喘发病率呈全球性增加已成为严重的公共卫生问题。非过敏原性空气污染物的增多与哮喘发病率的增加有密切关系，由我国室内空气领域著名学者杨旭提出的过敏体质激发原学说很好地解释了这一现象。随着城市化加快，臭氧污染已成为全球空气污染突出的问题。作为非过敏原性空气污染物，臭氧和哮喘的发生发展有确切的因果关系，但分子机制仍未明了。本项目提出臭氧是一种过敏体质激发原，获得性过敏体质是其诱发过敏性哮喘可能的机制。本项目开展整体动物实验和细胞实验，探讨臭氧的过敏体质激发原作用和通过以肥大细胞为起点的瞬时受体电位香草酸亚型1信号传递系统诱发过敏性哮喘，采用CPZ阻断该信号系统，通过对Ca2+、IL-4、IgE和肺功能、肺组织病理学、BALF炎症细胞分布、Th1/Th2平衡的分析，揭示臭氧诱发过敏性哮喘作用的分子机理，为将来早期识别臭氧敏感人群，强化哮喘防治措施提供理论依据。

哮喘发病率呈全球性上升趋势已成为严重的公共卫生问题。非过敏原性空气污染物的增多与哮喘发病率的增加有密切关系，过敏体质激发原学说很好地解释了这一现象。随着城市化加快，臭氧污染已成为全球空气污染突出的问题。作为非过敏原性空气污染物，臭氧和哮喘的发生发展有确切的因果关系。本项目提出臭氧是一种过敏体质激发原，获得性过敏体质是其诱发过敏性哮喘可能的机制。本项目建立了臭氧诱导型过敏性哮喘小鼠模型，采用CPZ阻断TRPV1信号系统，通过对IL-4、IgE等分子指标和肺功能、肺组织病理学、BALF炎症细胞分布、Th1/Th2平衡的分析，发现1ppm臭氧(3h*7d)具有过敏体质激发原作用和通过以肥大细胞为起点的瞬时受体电位香草酸亚型1信号传递系统诱发过敏性哮喘。该项目为将来早期识别臭氧敏感人群，强化哮喘防治措施提供理论依据。