REGULATION OF PULMONARY SURFACTANT SYSTEM AND ITS MODIFICATION BY TOXIC AGENTS

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Pulmonary surfactant is a heterogeneous complex consisting of surface active phospholipids and specific proteins synthesized and secreted by Type II cells in the alveoli of the lungs. The major lipid component of surfactant is dipalmitoylphosphatidylcholine and the major protein component is surfactant protein A (SPA) . SPA is a specific surfactant-associated protein found only in the lungs. The function of DPPC is to lower surface tension at the air/cell interface and the function of SPA appears to be to assist in this process. Biosynthesis and secretion of these substances by alveolar Type II cells is critical for the stabiliza- tion and function of the lungs. Silica dust causes massive increases in the pulmonary content of both surfactant phospholipids and proteins. The induction of surfactant production in the lungs appears to be a result of the silica-induced inflammatory condition and the mechanism through which this occurs is currently under investigation. Some, but not all , Type II calls within the alveoli become hypertrophic and we have shown that these type II cells are in an activated state with regards to their ability to synthesize both surfactant phospholipids and SPA. These hypertrophic Type II cells are responsible for the massive increases in surfactant found in the lungs of silica-exposed rats. At the present time we are trying to determine the mechanism through which intratracheal injection of silica leads to activation of alveolar type II cells.