title: Anti-c-Fms antibody inhibits lipopolysaccharide-induced osteoclastogenesis in vivo.
abstract: It has been reported that lipopolysaccharide (LPS) has the ability to induce inflammation and osteoclastogenesis. Osteoclast formation is dependent on macrophage-colony-stimulating factor (M-CSF) and ligand for the receptor activator of necrosis factor-kB. In this study, the effect of antibody against c-Fms, which is the receptor of M-CSF, on LPS-mediated osteoclastogenesis was investigated in mice. LPS was administered with or without anti-c-Fms antibody into the supracalvaria of mice. The number of osteoclasts and the levels of mRNA for cathepsin K and tartrate-resistant acid phosphatase, which are osteoclast markers, in mice administered both LPS and anti-c-Fms antibody were lower than those in mice administered LPS alone. The level of tartrate-resistant acid phosphatase 5b as a marker of bone resorption in mice administered both LPS and anti-c-Fms antibody was also lower. Furthermore, the expression of the receptor activator of necrosis factor-kB, which is receptor activator of nuclear factor kappa-B ligand, was increased upon LPS administration, but the expression was inhibited by anti-c-Fms antibody. These results showed that anti-c-Fms antibody inhibits LPS-induced osteoclast formation. In conclusion, M-CSF and its receptor are potential therapeutic targets in bacterial infection-induced osteoclastogenesis, and anti-c-Fms antibody might be useful for inhibition of bacterial infection-induced bone destruction.
authors: Division of Orthodontics and Dentofacial Orthopedics, Department of Translational Medicine, Tohoku University Graduate School of Dentistry, Sendai, Japan.
authors: Keisuke
authors: K
authors: Kimura
authors: Hideki
authors: H
authors: Kitaura
authors: Toshiya
authors: T
authors: Fujii
authors: Zaki Weli
authors: ZW
authors: Hakami
authors: Teruko
authors: T
authors: Takano-Yamamoto
mesh_terms: D000135:Acid Phosphatase / Q000235:genetics / Q000378:metabolism; D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology / Q000494:pharmacology*; D001862:Bone Resorption / Q000139:chemically induced / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D056657:Cathepsin K / Q000235:genetics / Q000378:metabolism; D006651:Histocytochemistry; D007527:Isoenzymes / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D016173:Macrophage Colony-Stimulating Factor / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010010:Osteoclasts / Q000166:cytology* / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D053246:Receptor Activator of Nuclear Factor-kappa B / Q000235:genetics / Q000378:metabolism; D016186:Receptor, Macrophage Colony-Stimulating Factor / Q000037:antagonists & inhibitors / Q000276:immunology* / Q000378:metabolism; D012886:Skull / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D000071681:Tartrate-Resistant Acid Phosphatase
chemical_list: D000911:Antibodies, Monoclonal; D007527:Isoenzymes; D008070:Lipopolysaccharides; D053246:Receptor Activator of Nuclear Factor-kappa B; C505687:Tnfrsf11a protein, mouse; D016173:Macrophage Colony-Stimulating Factor; D016186:Receptor, Macrophage Colony-Stimulating Factor; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase; D056657:Cathepsin K