Open Access
Article

Effects of acute ozone exposure on lung peak allergic inflammation of mice

Aihua Bao1,Li Liang1,Feng Li1,Min Zhang1,Xin Zhou1,*
1
Department of respiratory medicine, The Affiliated First People’s Hospital of Shanghai Jiaotong University, Shanghai 200080, China
DOI: 10.2741/4147 Volume 18 Issue 3, pp.838-851
Published: 01 June 2013
*Corresponding Author(s):  
Xin Zhou
E-mail:  
xzhou53@yeah.net
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.

Key words

Airway Hyperresponsiveness, Epithelial Injury, Hyaluronan, Inflammation, Mucus Hyperproduction, Ozone

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Aihua Bao, Li Liang, Feng Li, Min Zhang, Xin Zhou. Effects of acute ozone exposure on lung peak allergic inflammation of mice. Frontiers in Bioscience-Landmark. 2013. 18(3); 838-851.