Department of Respiratory Medicine, The Affiliated First People's Hospital of Shanghai Jiaotong University, Shanghai 200080, China.
Front Biosci (Landmark Ed). 2013 Jun 1;18(3):838-51. doi: 10.2741/4147.
Asthma exacerbations are often triggered by air pollution, including O3, whereas how patients with asthma exacerbations react to high levels of ambient ozone remain unknown. Here, we investigated the manner in which acute ozone exposure affects the pathophysiological characteristics of an asthma model on the premise of culminated allergic airway inflammation. The asthma model was constructed in mice, and enhanced pause (Penh), total and differential cell number, soluble mediator concentration, histopathology, and Muc5ac mRNA expression in the mice were observed. The results showed that ozone could induce airway hyperresponsiveness (AHR) in controls and an additional enhancement of preexisting AHR in asthmatic mice. When exposed to ozone, the asthmatic mice expressed more neutrophils, TNF-α, IL-13, and hyaluronan in bronchoalveolar lavage than controls. The mice with asthma and the controls both showed decreased epithelial cell density in the proximal and distal airways. Ozone aggravated the increased mucus production and mucin gene expression in mice with asthma. These results show that subjects with asthma may react differently to the same high level of ambient ozone, especially for those with asthma exacerbations.
哮喘发作通常是由空气污染引发的，包括 O3，而哮喘发作患者对环境臭氧水平升高的反应尚不清楚。在这里，我们在过敏气道炎症达到高峰的前提下，研究了急性臭氧暴露对哮喘模型病理生理特征的影响方式。在小鼠中构建了哮喘模型，并观察了增强呼气暂停（Penh）、总细胞和分类细胞数、可溶性介质浓度、组织病理学和小鼠 Muc5ac mRNA 表达。结果表明，臭氧可诱导对照小鼠气道高反应性（AHR），并在哮喘小鼠中进一步增强原有 AHR。暴露于臭氧时，哮喘小鼠在支气管肺泡灌洗液中的中性粒细胞、TNF-α、IL-13 和透明质酸的表达高于对照组。哮喘小鼠和对照组的近端和远端气道上皮细胞密度均降低。臭氧加重了哮喘小鼠的黏液产生增加和粘蛋白基因表达增加。这些结果表明，哮喘患者可能对相同水平的环境臭氧有不同的反应，尤其是那些哮喘发作的患者。
