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Published ahead of print on May 28, 2003, doi:10.1164/rccm.200212-1440OC

Am. J. Respir. Crit. Care Med., Volume 168, Number 3, August 2003, 335-341

A more recent version of this article appeared on August 1, 2003
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Submitted on December 12, 2002
Accepted on May 15, 2003

Cellular Anti-endotoxin Activities of Lung Surfactant Protein C in Lipid Vesicles

Luis A Augusto1, Monique Synguelakis1, Quentin Espinassous1, Michel Lepoivre2, Jan Johansson3, and Richard Chaby1*

1 Endotoxin Group, National Center for Scientific Research, Orsay, France, 2 Laboratory of Nitrogen Oxides Inflammation and Immunity, National Center for Scientific Research, Orsay, France, 3 Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden

* To whom correspondence should be addressed. 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 LPS 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 to vesicles of dipalmitoylphosphatidylcholine, SP-C inhibits the binding of a tritium-labeled lipopolysaccharide to the macrophage cell line RAW 264.7. In 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.
Key words: lipopolysaccharide, SP-C, tumor nectosis factor-alpha, nitric oxide, peroxynitrite




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