IL-12 Inhibits Lipopolysaccharide Stimulated Osteoclastogenesis in Mice
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...
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Journal of Immunology Research |
| Online Access: | http://dx.doi.org/10.1155/2015/214878 |
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| author | Masako Yoshimatsu Hideki Kitaura Yuji Fujimura Haruka Kohara Yukiko Morita Noriaki Yoshida |
| author_facet | Masako Yoshimatsu Hideki Kitaura Yuji Fujimura Haruka Kohara Yukiko Morita Noriaki Yoshida |
| author_sort | Masako Yoshimatsu |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-6ee6f5df29eb455b85568ee8696274b0 |
| institution | OA Journals |
| issn | 2314-8861 2314-7156 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
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| series | Journal of Immunology Research |
| spelling | doaj-art-6ee6f5df29eb455b85568ee8696274b02025-08-20T02:06:20ZengWileyJournal of Immunology Research2314-88612314-71562015-01-01201510.1155/2015/214878214878IL-12 Inhibits Lipopolysaccharide Stimulated Osteoclastogenesis in MiceMasako Yoshimatsu0Hideki Kitaura1Yuji Fujimura2Haruka Kohara3Yukiko Morita4Noriaki Yoshida5Department of Orthodontics and Dentofacial Orthopedics, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8588, JapanDivision of Orthodontics and Dentofacial Orthopedics, Department of Translational Medicine, Tohoku University Graduate School of Dentistry, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, JapanDepartment of Orthodontics and Dentofacial Orthopedics, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8588, JapanDepartment of Orthodontics and Dentofacial Orthopedics, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8588, JapanDepartment of Orthodontics and Dentofacial Orthopedics, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8588, JapanDepartment of Orthodontics and Dentofacial Orthopedics, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8588, JapanLipopolysaccharide (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.http://dx.doi.org/10.1155/2015/214878 |
| spellingShingle | Masako Yoshimatsu Hideki Kitaura Yuji Fujimura Haruka Kohara Yukiko Morita Noriaki Yoshida IL-12 Inhibits Lipopolysaccharide Stimulated Osteoclastogenesis in Mice Journal of Immunology Research |
| title | IL-12 Inhibits Lipopolysaccharide Stimulated Osteoclastogenesis in Mice |
| title_full | IL-12 Inhibits Lipopolysaccharide Stimulated Osteoclastogenesis in Mice |
| title_fullStr | IL-12 Inhibits Lipopolysaccharide Stimulated Osteoclastogenesis in Mice |
| title_full_unstemmed | IL-12 Inhibits Lipopolysaccharide Stimulated Osteoclastogenesis in Mice |
| title_short | IL-12 Inhibits Lipopolysaccharide Stimulated Osteoclastogenesis in Mice |
| title_sort | il 12 inhibits lipopolysaccharide stimulated osteoclastogenesis in mice |
| url | http://dx.doi.org/10.1155/2015/214878 |
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