Cellular antiendotoxin activities of lung surfactant protein C in lipid vesicles
| Autor: | Richard Chaby, Monique Synguelakis, Jan Johansson, Michel Lepoivre, Quentin Espinassous, Luis A. Augusto |
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| Rok vydání: | 2003 |
| Předmět: |
Pulmonary and Respiratory Medicine
Lipopolysaccharides Lipopolysaccharide Swine CD14 Lipopolysaccharide Receptors Antineoplastic Agents Biology In Vitro Techniques Critical Care and Intensive Care Medicine Nitric Oxide Nitric oxide Cell Line chemistry.chemical_compound Mice Pulmonary surfactant Macrophages Alveolar Animals Receptor Tumor Necrosis Factor-alpha Vesicle Cytoplasmic Vesicles Surfactant protein C Pulmonary Surfactants Free Radical Scavengers Pulmonary Surfactant-Associated Protein C Cell biology Endotoxins Disease Models Animal Biochemistry chemistry Macrophages Peritoneal Tumor necrosis factor alpha |
| Zdroj: | American journal of respiratory and critical care medicine. 168(3) |
| ISSN: | 1073-449X |
| Popis: | The respiratory system is continuously exposed to airborne particles containing lipopolysaccharide. Our laboratory established previously that the hydrophobic surfactant protein C (SP-C) binds to lipopolysaccharide and to one of its cellular receptors, CD14. Here we examined the influence of SP-C, and of a synthetic analog, on some cellular in vitro effects of lipopolysaccharide. When associated with vesicles of dipalmitoylphosphatidylcholine, SP-C inhibits the binding of a tritium-labeled lipopolysaccharide to the macrophage cell line RAW 264.7. Under similar conditions of presentation, SP-C inhibits the mitogenic effect of lipopolysaccharide on mouse splenocytes, and inhibits the lipopolysaccharide-induced production of tumor necrosis factor-alpha by peritoneal and alveolar macrophages, and of nitric oxide by RAW 264.7 cells. In contrast, tumor necrosis factor-alpha production induced by a lipopeptide, and nitric oxide production induced by picolinic acid, were not affected by SP-C. The lipopolysaccharide-binding capacity of SP-C is resistant to peroxynitrite, a known mediator of acute lung injury formed by reaction of nitric oxide with superoxide anions. These results indicate that SP-C may play a role in lung defense; SP-C resists degradation under inflammatory conditions and traps lipopolysaccharide, preventing it from inducing production of noxious mediators in alveolar cells. |
| Databáze: | OpenAIRE |
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