{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T23:09:05Z","timestamp":1774566545550,"version":"3.50.1"},"reference-count":60,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2003,8,1]],"date-time":"2003-08-01T00:00:00Z","timestamp":1059696000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2003,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>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-\u03b1 by peritoneal and alveolar macrophages, and of nitric oxide by RAW 264.7 cells. In contrast, tumor necrosis factor-\u03b1 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.<\/jats:p>","DOI":"10.1164\/rccm.200212-1440oc","type":"journal-article","created":{"date-parts":[[2003,6,3]],"date-time":"2003-06-03T21:21:44Z","timestamp":1054675304000},"page":"335-341","source":"Crossref","is-referenced-by-count":27,"title":["Cellular Antiendotoxin Activities of Lung Surfactant Protein C in Lipid Vesicles"],"prefix":"10.1093","volume":"168","author":[{"given":"Luis A.","family":"Augusto","sequence":"first","affiliation":[{"name":"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"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Monique","family":"Synguelakis","sequence":"additional","affiliation":[{"name":"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"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Quentin","family":"Espinassous","sequence":"additional","affiliation":[{"name":"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"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michel","family":"Lepoivre","sequence":"additional","affiliation":[{"name":"Endotoxin Group, and Laboratory 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