Source:http://linkedlifedata.com/resource/pubmed/id/20111957
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
2010-2-22
|
| pubmed:abstractText |
It has recently been reported that tumor necrosis factor (TNF)-alpha has the ability to accelerate osteoclastogenesis. We previously reported that the proinflammatory cytokine interleukin (IL)-18 inhibits TNF-alpha-mediated osteoclastogenesis in mouse bone marrow cultures. In the present study, the effect of IL-18 on TNF-alpha-mediated osteoclastogenesis was investigated in vivo. We administered TNF-alpha with or without IL-18 into the supracalvaria of mice. The number of osteoclasts in the suture of the calvaria was increased in mice administered TNF-alpha. The number of osteoclasts in mice administered both TNF-alpha and IL-18 was lower than that in mice administered TNF-alpha alone. We previously showed that IL-12 and IL-18 synergistically inhibit TNF-alpha-mediated osteoclastogenesis in vitro. To assess the ability of these two cytokines to synergistically inhibit TNF-alpha-induced osteoclastogenesis in vivo, mice were administered the two cytokines at doses that did not inhibit osteoclast formation. The combination of IL-12 and IL-18 markedly inhibited TNF-alpha-induced osteoclastogenesis in vivo. To evaluate how IL-12 and IL-18 synergistically affect TNF-alpha-induced osteoclastogenesis, the IL-18 receptor (IL-18R) and IL-12R expression levels were analyzed by RT-PCR in bone marrow cells cultured with IL-12 or IL-18. IL-18R mRNA was increased in cells cultured with IL-12, while IL-12R mRNA was increased in cells cultured with IL-18. In addition, IL-18 inhibited TNF-alpha-induced osteoclastogenesis in mice with T-cell depletion caused by anti-CD4 and anti-CD8 antibodies. The present results suggest that IL-18 may inhibit TNF-alpha-mediated osteoclastogenesis in vivo via a T cell-independent mechanism.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-18,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-18,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
1432-0827
|
| pubmed:author | |
| pubmed:issnType |
Electronic
|
| pubmed:volume |
86
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
242-8
|
| pubmed:meshHeading |
pubmed-meshheading:20111957-Animals,
pubmed-meshheading:20111957-Bone Remodeling,
pubmed-meshheading:20111957-Bone Resorption,
pubmed-meshheading:20111957-Cell Count,
pubmed-meshheading:20111957-Cell Differentiation,
pubmed-meshheading:20111957-Cell Proliferation,
pubmed-meshheading:20111957-Cells, Cultured,
pubmed-meshheading:20111957-Dose-Response Relationship, Drug,
pubmed-meshheading:20111957-Drug Synergism,
pubmed-meshheading:20111957-Interleukin-12,
pubmed-meshheading:20111957-Interleukin-18,
pubmed-meshheading:20111957-Male,
pubmed-meshheading:20111957-Mice,
pubmed-meshheading:20111957-Mice, Inbred C57BL,
pubmed-meshheading:20111957-Osteoclasts,
pubmed-meshheading:20111957-RNA, Messenger,
pubmed-meshheading:20111957-Receptors, Interleukin-12,
pubmed-meshheading:20111957-Receptors, Interleukin-18,
pubmed-meshheading:20111957-Stem Cells,
pubmed-meshheading:20111957-T-Lymphocytes,
pubmed-meshheading:20111957-Tumor Necrosis Factor-alpha,
pubmed-meshheading:20111957-Up-Regulation
|
| pubmed:year |
2010
|
| pubmed:articleTitle |
IL-18 inhibits TNF-alpha-induced osteoclastogenesis possibly via a T cell-independent mechanism in synergy with IL-12 in vivo.
|
| pubmed:affiliation |
Department of Orthodontics and Dentofacial Orthopedics, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|