Effect of NO2 exposure on airway inflammation and oxidative stress in asthmatic mice

Nitrogen dioxide (NO2) is a widespread air pollutant. Epidemiological evidence indicates that NO2 is associated with an increase of incidence rate and mortality of asthma, but its mechanism is still unclear. In this study, we exposed mice to NO2 (5 ppm, 4 h per day for 30 days) intermittently to investigate the development and potential toxicological mechanisms of allergic asthma. We randomly assigned 60 male Balb/c mice to four groups: saline control, ovalbumin (OVA) sensitization, NO2 alone, and OVA+NO2 groups. The involved mechanisms were found from the perspective of airway inflammation and oxidative stress. The results showed that NO2 exposure could aggravate lung inflammation in asthmatic mice, and airway remodeling was characterized by significant thickening of the airway wall and infiltration of inflammatory cells. Moreover, NO2 would aggravate the airway hyperresponsiveness (AHR), which is characterized by significantly elevated inspiratory resistance (Ri) and expiratory resistance (Re), as well as decreased dynamic lung compliance (Cldyn). In addition, NO2 exposure promoted pro-inflammatory cytokines (IL-6 and TNF-& alpha;) and serum immunoglobulin (IgE) production. The imbalance of Th1/Th2 cell differentiation (IL-4 increased, IFN-& gamma; reduced, IL-4/IFN-& gamma; significantly increased) played a key role in the inflammatory response of asthma under NO2 exposure. In a nutshell, NO2 exposure could promote allergic airway inflammation and increase asthma susceptibility. The levels of ROS and MDA among asthmatic mice exposed to NO2 increased significantly, while GSH levels sharply decreased. These findings may provide better toxicological evidence for the mechanisms of allergic asthma risk due to NO2 exposure.

Automated summary

This study investigates the potential toxicological mechanisms of allergic asthma caused by exposure to nitrogen dioxide (NO2) in mice. The results show that NO2 exposure aggravates lung inflammation and airway remodeling in asthmatic mice, as well as promotes airway hyperresponsiveness and inflammatory cytokine production. The imbalance of Th1/Th2 cell differentiation plays a key role in the inflammatory response of asthma under NO2 exposure.