Alice G Vassiliou1, Nikolaos Manitsopoulos1, Matina Kardara1, Nikolaos A Maniatis1,2, Stylianos E Orfanos3,2, Anastasia Kotanidou1,4. 1. GP Livanos and M. Simou Laboratories, First Department of Critical Care Medicine & Pulmonary Services, Evangelismos Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece. 2. Second Department of Critical Care, Attikon Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece. 3. GP Livanos and M. Simou Laboratories, First Department of Critical Care Medicine & Pulmonary Services, Evangelismos Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece sorfanos@med.noa.gr. 4. First Department of Critical Care Medicine & Pulmonary Services, National and Kapodistrian University of Athens Medical School, Evangelismos Hospital, Athens, Greece.
Abstract
AIM: The mammalian lung expresses at least three aquaporin (AQP) water channels whose precise role in lung injury or inflammation is still controversial. MATERIALS AND METHODS: Three murine models of lung inflammation and corresponding controls were used to evaluate the expression of Aqp1, Aqp4, Aqp5 and Aqp9: lipopolysaccharide (LPS)-induced lung injury; HCl-induced lung injury; and ventilation-induced lung injury (VILI). RESULTS: All models yielded increased lung vascular permeability, and inflammatory cell infiltration in the broncho-alveolar lavage fluid; VILI additionally produced altered lung mechanics. Lung expression of Aqp4 decreased in the models that targeted primarily the alveolar epithelium, i.e. acid aspiration and mechanical ventilation, while Aqp5 expression decreased in the model that appeared to target both the capillary endothelium and alveolar epithelium, i.e. LPS. CONCLUSION: Participation of aquaporins in the acute inflammatory process depends on localization and the type of lung injury. Copyright
AIM: The mammalian lung expresses at least three aquaporin (AQP) water channels whose precise role in lung injury or inflammation is still controversial. MATERIALS AND METHODS: Three murine models of lung inflammation and corresponding controls were used to evaluate the expression of Aqp1, Aqp4, Aqp5 and Aqp9: lipopolysaccharide (LPS)-induced lung injury; HCl-induced lung injury; and ventilation-induced lung injury (VILI). RESULTS: All models yielded increased lung vascular permeability, and inflammatory cell infiltration in the broncho-alveolar lavage fluid; VILI additionally produced altered lung mechanics. Lung expression of Aqp4 decreased in the models that targeted primarily the alveolar epithelium, i.e. acid aspiration and mechanical ventilation, while Aqp5 expression decreased in the model that appeared to target both the capillary endothelium and alveolar epithelium, i.e. LPS. CONCLUSION: Participation of aquaporins in the acute inflammatory process depends on localization and the type of lung injury. Copyright
Authors: John Villandre; Virginia White; Travis B Lear; Yanwen Chen; Ferhan Tuncer; Emily Vaiz; Beyza Tuncer; Karina Lockwood; Dan Camarco; Yuan Liu; Bill B Chen; John Evankovich Journal: Front Pharmacol Date: 2022-01-25 Impact factor: 5.988