哮喘联盟

   摘要
   哮喘急性发作通常由包括O3在内的空气污染所诱发，然而哮喘急性发作患者在高浓度臭氧环境中的反应仍不明确。本文研究了急性臭氧暴露对哮喘模型中处于过敏性气道炎症高峰者的病理生理特征的影响。以小鼠建立哮喘模型，观察小鼠增强的呼吸间歇(Penh)、总的和分类细胞数、可溶性介质浓度、组织病理学和Muc5ac mRNA的表达。结果显示，对照组中臭氧可诱导气道高反应性，在哮喘小鼠中，臭氧额外增强了已有的气道高反应性。当处于臭氧暴露时，通过支气管肺泡灌洗，哮喘小鼠与对照组相比表达出更多的中性粒细胞、TNF-α、IL-13和透明质酸。哮喘小鼠和对照组均显示出了气道近端和远端上皮细胞密度的减少。臭氧加重哮喘小鼠粘液分泌的增加和粘蛋白基因的表达。这些结果说明哮喘受试小鼠在同样高水平的臭氧环境中反应不同，尤其是那些哮喘急性发作者。

 

（刘国梁 审校）
Front Biosci. 2013 Jun 1;18:838-51.

 

Consequences of acute ozone exposure imposed on the culminated allergic pulmonary inflammation in an established murine model of asthma.
 

Bao A, Liang L, Li F, Zhang M, Zhou X.
 

Abstract
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.

Front Biosci. 2013 Jun 1;18:838-51.