Abstract:

Objective To observe the allergic airway inflammation and lung pathology in mice with asthma induced by nitrated pollen. Methods Sixty mice were randomly divided into 5 groups according to different sensitization and challenge. Group A to group D were asthma model groups, and group E was normal control group. The right lung tissues of mice were obtained, the pathological changes of lung tissues were observed with HE staining, and the tracheal wall thickness (total wall area/basement membrane perimeter, WAt/Pbm) and airway smooth muscle thickness (smooth muscle area/basement membrane perimeter, WAm/Pbm) were calculated. The cytological changes in bronchoalveolar lavage fluid (BALF) were observed, the level of nuclear factor kappa B (NF-κB) p65 activation and expression of 3-nitrotyrosine (3-NT) in lung tissues were determined by immunohistochemical method, and the apoptosis of eosinophils (EOS) in lung tissues was detected by TUNEL. Results The numbers of white cells, EOS and neutrophil (NEU) and percents of them in total cells in BALF, WAt/Pbm and WAm/Pbm, the level of NF-κB p65 activation and expression of 3-NT in each asthma model group were significantly higher than those in group E (P<0.01), while the apoptosis rate of eosinophils in lung tissues in each group was significantly lower than that in group E (P<0.01). Compared with the other model groups, the values of those indicators in group D in which mice were immunized and challenged with nitrated pollen changed more significantly (P<0.05 or P<0.01). Pearson correlation analysis revealed that the expression of 3-NT was significantly negatively correlated with apoptosis rate of EOS (r=－0.632, P<0.05), and was significantly positively correlated with the level of NF-κB p65 activation (r=0.667, P<0.05). Conclusion High level of oxidative stress which exists in asthmatic mice immunized and challenged with nitrated pollen may elevate the expression of 3-NT, activate NF-κB signaling pathway, delay apoptosis of EOS, and result in more severe airway inflammation and pathological changes.

Key words: air pollution, pollen, asthma, oxidative stress, inflammation