Decreased expression of aquaporin (AQP)1 and AQP5 in mouse lung after acute viral infection

Intratracheal infection of mice with adenovirus is associated with subseque nt pulmonary inflammation and edema. Water movement through the air space-c apillary barrier in the distal lung is facilitated by aquaporins (AQPs). To investigate the possibility that distal lung AQPs undergo altered regulati on under conditions of aberrant fluid handling in the lung, we analyzed mes senger RNA (mRNA) and protein expression of AQPs 1 and 5 in the lungs of mi ce 7 and 14 d after infection with adenovirus. Here, we demonstrate that AQ P1 and AQP5 show decreased expression following adenoviral infection, North ern blot analysis showed significantly decreased mRNA levels of AQP1, which is expressed in the capillary endothelium, and AQP5, which is expressed in alveolar epithelium, in the lungs of mice both 7 and 14 d after infection. Immunoblotting studies demonstrated significantly reduced levels of AQP1 a nd AQP5 protein after infection as well. In addition, mRNA expression of th e alpha subunit of the epithelial sodium channel was reduced in the lungs o f mice 7 and 14 d after adenoviral infection. In contrast, mRNA expression of the alpha 1 subunit of the Na,K-adenosine triphosphatase in the lung was unaltered. Immunohistochemical analysis demonstrated that the decreases in AQP1 and AQP5 expression were not localized to regions of overt inflammati on hut were found throughout the lung. Thus, this study provides the first report of AQP gene regulation in an in vivo model of pulmonary inflammation and edema. Decreased AQP 1 and AQP5 levels during adenoviral infection sug gest a role for AQP1 and AQP5 in the abnormal fluid fluxes detected during pulmonary inflammation.