Ozone inhalation induces exacerbation of eosinophilic airway inflammation and Th2-skew immune response in a rat model of AR

Ozone (O3) exposure elicits allergic rhinitis (AR) exacerbations by mechanisms that remain poorly understood. We used a rat model to investigate the effects of O3 on eosinophilic airway inflammation and Th2-related response. Sprague-Dawley (SD) rats were sensitized and challenged with ovalbumin (OVA) to make AR models. Three groups of AR rats were exposed respectively to 0.5, 1.0, 2.0 ppm of O3 for 2 h daily over 6 weeks consecutively and studied 24 h later. Normal rats exposed to O3 alone were used as controls. Nasal symptoms and OVA-specific immunoglobulin E (OVA-sIg E) in the serum were evaluated. Inflammatory cells in nasal lavage fluid (NLF) were classified and counted. Cytokines protein levels in NLF were assessed by ELISA. The pathological changes in the nasal mucosa were examined by histology. The combination of allergen and repeated O3 exposure in rats induced a significant increase of the number of sneezes, nasal rubs, amount of nasal secretion and OVA-sIgE in the serum, accompanied by enhancement of eosinophils in NLF and nasal mucosa. The increase of interleukin-5 (IL-5), IL-13, Eotaxin and decrease of INF-γ protein levels in NLF were detected in AR rats after O3 inhalation. Hematoxylin and eosin staining showed disordered arrangement of the nasal mucosa epithelium and eosinophilic infiltration in a concentration-dependent manner. O3 inhalation deteriorated symptoms in AR rats, and the possible mechanism is that ozone co-exposure could enhance the expression of Th2 cytokines, eosinophilic airway inflammation dose-dependently. The observation is helpful for us to understand the synergistic effect of O3 in the air pollution and allergen on aggravating allergic rhinitis.