title: Decreased expression of aquaporin (AQP)1 and AQP5 in mouse lung after acute viral infection.
abstract: 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.
authors.affiliation: Department of Molecular Genetics, Biochemistry and Microbiology, College of Medicine, University of Cincinnati, Ohio 45267-0524, USA.
authors.forename: J E
authors.initials: JE
authors.lastname: Towne
authors.forename: K S
authors.initials: KS
authors.lastname: Harrod
authors.forename: C M
authors.initials: CM
authors.lastname: Krane
authors.forename: A G
authors.initials: AG
authors.lastname: Menon
mesh_terms: D000256:Adenoviridae / Q000235:genetics*; D000257:Adenoviridae Infections / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D051398:Aquaporin 1; D051402:Aquaporin 5; D020346:Aquaporins / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D005822:Genetic Vectors / Q000008:administration & dosage; D007150:Immunohistochemistry; D007442:Intubation, Intratracheal; D008168:Lung / Q000378:metabolism* / Q000648:ultrastructure / Q000821:virology; D008565:Membrane Proteins; D051379:Mice; D008815:Mice, Inbred Strains; D008854:Microscopy, Electron; D011654:Pulmonary Edema / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D012333:RNA, Messenger / Q000096:biosynthesis; D012141:Respiratory Tract Infections / Q000378:metabolism / Q000473:pathology / Q000821:virology
chemical_list: C496021:Aqp1 protein, mouse; C496038:Aqp5 protein, mouse; D051402:Aquaporin 5; D020346:Aquaporins; D008565:Membrane Proteins; D012333:RNA, Messenger; D051398:Aquaporin 1