Intratracheal
infection of mice with adenovirus is associated with subsequent
pulmonary inflammation and
edema. Water movement through the air space-capillary barrier in the distal lung is facilitated by
aquaporins (AQPs). To investigate the possibility that distal lung AQPs undergo altered regulation under conditions of aberrant fluid handling in the lung, we analyzed
messenger RNA (
mRNA) and
protein expression of AQPs 1 and 5 in the lungs of mice 7 and 14 d after
infection with adenovirus. Here, we demonstrate that AQP1 and AQP5 show decreased expression following adenoviral
infection. Northern 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 and
AQP5 protein after
infection as well. In addition,
mRNA expression of the alpha subunit of the
epithelial sodium channel was reduced in the lungs of mice 7 and 14 d after adenoviral
infection. In contrast,
mRNA expression of the alpha1 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
inflammation but 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 AQP1 and AQP5 levels during adenoviral
infection suggest a role for AQP1 and AQP5 in the abnormal fluid fluxes detected during
pulmonary inflammation.