The mammalian peripheral lung contains at least three aquaporin (Aqp) water channels: Aqp1 in microvascular endothelia, Aqp4 in airway epithelia, and Aqp5 in alveolar epithelia. These aquaporins play a major role in osmotic water movement and participate in edema formation, however, their precise role in lung injury or inflammation is still controversial. Three murine (8-10 week old C57/BL6) models of lung inflammation and corresponding controls (n= 9/group) were used to evaluate the expression of Aqps: I) LPS-induced lung injury; intratracheal instillation (it) of normal saline (NS) or LPS (5mg/kg), II) HCl-induced lung injury; it NS or 0.1N HCl. Animals of groups I & II were sacrificed 24hrs post-treatment. III) Ventilation-induced lung injury (VILI); tidal volumes of 8ml/kg or 25ml/kg; mice were sacrificed after 4hrs of mechanical ventilation. Following sacrifice lung tissues were obtained and snap frozen in liquid nitrogen. Aqp1, 4 and 5 mRNAs were quantified by real-time PCR and protein levels were measured by immunoblotting. All models yielded increased lung vascular permeability and inflammatory cell infiltration in the bronchoalveolar lavage fluid; VILI additionally produced altered lung mechanics. Aqp1 expression remained unaltered; Aqp4 decreased in HCl-induced lung injury and VILI and Aqp5 tended to increase, whereas it decreased in the LPS model. These results show that Aqp4 decreases and Aqp5 tends to increase in the models that target primarily the alveolar epithelium, i.e. acid aspiration and mechanical ventilation, while Aqp5 decreases in the model that targets primarily the capillary endothelium, i.e. LPS, indicating that participation of Aqps in the acute inflammatory process is location and type of lung injury specific.