Methods: The experimental design was approved by the Ethics Committee of Federal University of Ouro Preto (UFOP)-No.092/2012. Groups of female BALB⁄c mice (8 weeks old; 24.53±0.31g) were divided randomly in to five experimental groups as follows: Control group (CG) remained to air room; PBS group received aluminum hydroxide in phosphate buffered saline (PBS); OVA group (OVA) received ovalbumin and aluminum hydroxide in PBS; O2 group (O2) was exposed to 100% oxygen in a chamber for 24h; OVA+O2 group (OVA+O2) was exposed to 100% oxygen for 24h, received ovalbumin and aluminum hydroxide in PBS. The data were presented as the mean ± standard error of the mean. For continuous data, we used a One-Way Anova followed by the Student–Newman–Keuls post hoc test. For non-continuous data, we used the Kruskal–Wallis test followed by the Dunn’s post hoc test. In all instances, the significance level was set at 5% (p<0.05).
Results: In bronchoalveolar lavage the hyperoxia decreases macrophage number in O2 (2.82±0.20) and OVA+O2 (1.72±0.15) and increases neutrophils number in O2 (1.79±0.13) and OVA+O2 (1.72±0.15), compared to CG (macrophage: 5.36±0.33) and (neutrophils: 0.02±0.00). The Lymphocytes number were higher in O2 (1.08±0.07) and OVA+O2 (0.97±0.08) compared to CG (0.43±0.02). When the animals were exposed to oxygen and ovalbumin, concomitantly (OVA+O2 - 4.55±0.23), the hyperoxia decreases lymphocytes number when compared to OVA (4.55±0.23). The TNF-alpha content were higher in PBS (134.00±7.03), OVA (126.30±3.40), O2 (141.60±6.08) and OVA+O2 (129.60±5.05) when compared to CG (94.67±2.03). In lung sections, the hyperoxia increases interleukin-17 in airway epithelial cells, alveolar type II cells and alveolar macrophages after ovalbumin-induced lung inflammation. When the animals were exposed to oxygen and ovalbumin, concomitantly, the staining with IL17 were increase when compared to OVA (p<0.001).
Conclusions: Hyperoxia-induced oxidative stress increases IL17 in airway epithelial cells, alveolar type II cells and alveolar macrophages after ovalbumin-induced lung inflammation.