Different isoforms of glutathione peroxidase cause opposing effects during the development of allergic asthma in mice.

摘要

Recent studies identified increased levels of oxidative stress and alterations of antioxidant enzymes in the lungs of asthmatic individuals and in experimental animal models, suggesting that the increase in oxidative stress may significantly contribute to the characteristic features of allergic respiratory diseases (1). Won et al. (9) as well as our own work (4) focused on the role of glutathione peroxidases (GPx) in the development of experimental allergic asthma in mice. After allergen sensitization and subsequent airway challenges with ovalbumin of GPxl knock-out mice, Won et al. observed an attenuation of allergen-induced eosinophilic infiltration and airway hyperresponsiveness compared with wild-type mice. In our asthma mouse model, we showed that GPx2 knock-out mice behaved in the exact opposite way: ovalbumin airway challenges after sensitization induced increased allergen eo-sinophil inflammation and airway hyperreactivity compared with the corresponding wild-type mice. Taken together, these results indicate that different GPx activities cause opposing effects during the development of allergic asthma.