title: IL-12 Inhibits Lipopolysaccharide Stimulated Osteoclastogenesis in Mice.
abstract: Lipopolysaccharide (LPS) is related to osteoclastogenesis in osteolytic diseases. Interleukin- (IL-) 12 is an inflammatory cytokine that plays a critical role in host defense. In this study, we investigated the effects of IL-12 on LPS-induced osteoclastogenesis. LPS was administered with or without IL-12 into the supracalvariae of mice, and alterations in the calvarial suture were evaluated histochemically. The number of osteoclasts in the calvarial suture and the mRNA level of tartrate-resistant acid phosphatase (TRAP), an osteoclast marker, were lower in mice administered LPS with IL-12 than in mice administered LPS alone. The serum level of tartrate-resistant acid phosphatase 5b (TRACP 5b), a bone resorption marker, was also lower in mice administered LPS with IL-12 than in mice administered LPS alone. These results revealed that IL-12 might inhibit LPS-induced osteoclastogenesis and bone resorption. In TdT-mediated dUTP-biotin nick end-labeling (TUNEL) assays, apoptotic changes in cells were recognized in the calvarial suture in mice administered LPS with IL-12. Furthermore, the mRNA levels of both Fas and FasL were increased in mice administered LPS with IL-12. Taken together, the findings demonstrate that LPS-induced osteoclastogenesis is inhibited by IL-12 and that this might arise through apoptotic changes in osteoclastogenesis-related cells induced by Fas/FasL interactions.
authors.affiliation: Department of Orthodontics and Dentofacial Orthopedics, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8588, Japan.
authors.forename: Masako
authors.initials: M
authors.lastname: Yoshimatsu
authors.affiliation: Division of Orthodontics and Dentofacial Orthopedics, Department of Translational Medicine, Tohoku University Graduate School of Dentistry, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan.
authors.forename: Hideki
authors.identifier: 0000-0003-3249-4247
authors.initials: H
authors.lastname: Kitaura
authors.affiliation: Department of Orthodontics and Dentofacial Orthopedics, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8588, Japan.
authors.forename: Yuji
authors.initials: Y
authors.lastname: Fujimura
authors.affiliation: Department of Orthodontics and Dentofacial Orthopedics, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8588, Japan.
authors.forename: Haruka
authors.initials: H
authors.lastname: Kohara
authors.affiliation: Department of Orthodontics and Dentofacial Orthopedics, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8588, Japan.
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Morita
authors.affiliation: Department of Orthodontics and Dentofacial Orthopedics, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8588, Japan.
authors.forename: Noriaki
authors.initials: N
authors.lastname: Yoshida
mesh_terms: D000135:Acid Phosphatase / Q000276:immunology; D000818:Animals; D002454:Cell Differentiation / Q000276:immunology; D053222:Fas Ligand Protein / Q000276:immunology; D018664:Interleukin-12 / Q000276:immunology*; D007527:Isoenzymes / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010010:Osteoclasts / Q000276:immunology*; D010012:Osteogenesis / Q000276:immunology*; D012333:RNA, Messenger / Q000276:immunology; D000071681:Tartrate-Resistant Acid Phosphatase; D019014:fas Receptor / Q000276:immunology
chemical_list: D053222:Fas Ligand Protein; D007527:Isoenzymes; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D019014:fas Receptor; D018664:Interleukin-12; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase