Interactions of surfactant protein A with epithelial cells and phagocytes

• Published in: BBA - Molecular Basis of Disease 1998-11, Vol.1408 (2), p.241-263
• Main Authors: Tino, MichaelJames, Wright, JoRae
• Format: Article
• Language: English
• Subjects: Alveolar epithelium; Alveolar macrophage; Epithelial Cells - metabolism; Models, Biological; Monocyte; Phagocytes - immunology; Phagocytes - metabolism; Phagocytosis; Protein Binding; Proteolipids - isolation & purification; Proteolipids - metabolism; Pulmonary Alveoli - cytology; Pulmonary Alveoli - metabolism; Pulmonary surfactant; Pulmonary Surfactant-Associated Protein A; Pulmonary Surfactant-Associated Proteins; Pulmonary Surfactants - isolation & purification; Pulmonary Surfactants - metabolism; Receptors, Cell Surface - metabolism; Surfactant protein A
• ISSN: 0925-4439; 0006-3002; 1879-260X
• DOI: 10.1016/S0925-4439(98)00071-4

Surfactant protein A (SP-A) has been shown to bind to and regulate the functions of both alveolar type II cells and immune cells including alveolar macrophages. The interaction of SP-A with type II cells has been shown in vitro to inhibit lipid secretion and to promote the uptake of lipid by these cells and these observations led to the hypothesis that SP-A plays an important role in regulating surfactant turnover and metabolism. The finding that mice made deficient in SP-A by homologous recombination (SP-A −/− mice) have relatively normal surfactant pool sizes has raised the possibility that either redundant mechanisms function in vivo to keep pool sizes normal in the absence of SP-A or that the in vitro findings are not significant in the context of the whole, unstressed animal. The interaction of SP-A with immune cells has been shown to affect a variety of responses which, in general, function to promote host defense against infection. Although SP-A receptors have been identified, additional studies will be required to elucidate the mechanism of interaction of SP-A with these cells and the relative importance of the different receptors in SP-A mediated regulation of cell function.