期刊
INFLAMMATION
卷 37, 期 3, 页码 657-669出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-013-9782-0
关键词
inflammation; bone metabolism; osteoblast; osteoclast; apoptosis
资金
- Ministry of Education, Culture, Sports, Science, and Technology (MEXT), Tokyo, Japan [20791628]
- Aichi Gakuin University High-Tech Research Center (Aichi, Japan) Project for Private Universities from MEXT
- Grants-in-Aid for Scientific Research [24792342, 20791628, 24593134] Funding Source: KAKEN
This study analyzes the effect of interleukin-15 (IL-15) on osteoclast formation using a coculture of mouse osteoblasts and bone marrow cells (BMCs) stimulated with prostaglandin E2 (PGE(2)), which both have important role in rheumatoid arthritis (RA) and periodontal disease (PD). BMCs isolate lacking T (BMT-) or NK (BMNK-) cells, BMCs with no cells removed (BMT+NK+), purified NK cells, and purified T cells were each cocultured with osteoblasts in the presence or absence of PGE(2) and/or IL-15. The number of both osteoclasts and osteoblasts was decreased by IL-15 in a dose-dependent manner in BMT+NK+, BMT-. However, the reductions were improved in BMNK-. The expression of caspase3 in osteoblasts cocultured with NK cells was increased in a dose-dependent manner by IL-15. IL-15 stimulates apoptosis of osteoblasts via activation of NK cells. Since osteoblasts have an important role in bone formation, IL-15 may be an inflammatory bone destructive factor in RA and PD.
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