AQP5 role in ovalbumin-induced airway inflammation and secretion of MUC5AC in mice

Background: Airway inflammation and mucus hypersecretion are two important characteristic features of the pathogenesis of asthma. Aquaporin5 (AQP5) is known to be a water channel protein expressed widely in lung epithelium and submucosal glands. Objective: The present study aimed at investigating the involvement of AQP5 in asthma. Methods: The ovalbumin (OVA)-induced allergic pulmonary inflammation and MUC5AC production were examined in AQP5 +/+ or AQP5 –/– mice. The expression of AQPs in lung tissue and their regulation were detected. In addition, epidermal growth factor receptor (EGFR) expression and osmotic water permeability in lung were evaluated. Results: Lower expression of AQP1, 4, 5 while higher AQP3 was significant in lung tissue from AQP5 +/+ model mice. Only AQP1 and AQP5 were up-regulated by anti-asthmatic agents (dexamethasone, ambroxol and terbutaline) significantly. However, AQP5 knockout had significantly low airway inflammation and less lung edema induced by OVA, as compared with those in AQP5 +/+ mice. In addition, lower expression of MUC5AC in airway epithelium, less secretion of MUC5AC were found in AQP5 –/– model mice. Moreover, the expression of EGFR on airway epithelium was prevented by AQP5 knockout in asthmatic model. Conclusion: Our data indicate that AQP5 is involved in the development of allergic airway inflammation and mucus hypersecretion by regulating osmotic water permeability and expression of EGFR.