Lungs provide a mechanism for oxygen to access blood.
Diffusion of oxygen from lung alveoli into capillary blood requires a thin blood-gas barrier consisting of only alveolar epithelial cells and capillary endothelial cells. Lung inflammation disrupts the endothelial cell barrier and allows fluid, molecules and white blood cells to leak into the interstitium between endothelial cells and epithelial cells, thus decreasing blood oxygenation. The focus of our laboratory is to identify cellular mechanisms promoting endothelial cell disruption during lung inflammation so that we can hopefully develop pharmacologic agents useful in the treatment of inflammatory lung disorders. Lung endothelial cells normally form a continuous sheet in which each cell contacts two or three neighboring cells. In response to inflammatory agents like circulating neurohumoral mediators, oxidants, cytokines, and bacterial components, endothelial cells lose close contact with their neighbors and form transient gaps in the sheet.