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Cellular Antiendotoxin Activities of Lung Surfactant Protein C in Lipid Vesicles

Endotoxin Group, and Laboratory of Nitrogen Oxides Inflammation and Immunity, UMR-8619, National Center for Scientific Research, University of Paris-Sud, Orsay, France; and Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden

Correspondence and requests for reprints should be addressed to Richard Chaby, M.D., Equipe Endotoxines, UMR-8619 du CNRS, Bâtiment 430, Université de Paris-Sud, 91405 Orsay, France. E-mail: richard.chaby{at}bbmpc.u-psud.fr

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- by peritoneal and alveolar macrophages, and of nitric oxide by RAW 264.7 cells. In contrast, tumor necrosis factor- 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.

Key Words: lipopolysaccharide • nitric oxide • peroxynitrite • surfactant protein-C • tumor necrosis factor-

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