Surfactant and acute lung injury.

Abstract

This brief review will emphasize four interconnected pathways that can lead to functional abnormalities of surfactant that contribute to lung mechanics and gas exchange abnormalities in acute lung injury. Type II cells, the cells that make and secrete all of the lipids and proteins in surfactant, can be injured, resulting in disruption of metabolic pathways. The normal alveolar conversion of surfactant from active to inactive forms can accelerate with lung injury to deplete the active alveolar pool of surfactant. Alveolar-capillary damage from mechanical ventilation or cytokines will result in interstitial and alveolar edema, and alveolar edema can inhibit surfactant function by a variety of mechanisms. The host defense systems in the lung include macrophages and surfactant protein-A (SP-A). Injury can result in SP-A depletion, macrophage activation, and migration of activated granulocytes into the lungs with release of inflammatory cytokines, oxidants, and proteases that can interfere with surfactant function.