Abstract
Alveolar epithelial barrier dysfunction contributes to the influx of protein-rich edema fluid and the accumulation of inflammatory cells in the pathogenesis of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). To study the alveolar epithelial barrier function under pathological conditions, we developed an in vitro model of acute lung injury using cultured human alveolar epithelial type II (ATII) cells. Here we describe the methods that we use to measure protein permeability and fluid transport across human ATII cell monolayers under stimulated conditions. Both proinflammatory cytokines and edema fluid from ALI/ARDS patients can increase protein permeability and decrease fluid transport across the human ATII cells monolayer.
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