| Project/Area Number |
17K11686
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | Nihon University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
三上 剛和 新潟大学, 医歯学系, 准教授 (80434075)
好士 亮介 日本大学, 歯学部, 専修研究員 (80453877)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 細胞死 / 関節リウマチ / 歯肉上皮 / 三次元培養系 / 短鎖脂肪酸 / オートファジー / 活性酸素種 / 歯周炎 / DAMPs / 三次元培養 / 歯周疾患 / 自己免疫疾患 |
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| Outline of Final Research Achievements |
Rheumatoid arthritis (RA) is thought to be associated with periodontal disease. We previously demonstrated that butyrate, a short-chain fatty acid, which is produced by periodontopathic bacteria, induces death of human gingival epithelial cells, resulting in release of molecules that are important for RA onset. The aim of this study is to prove the death-inducing mechanisms by butyrate and other short-chain fatty acids. Not only butyrate, propionate, isobutyrate, and isovalerate also induced death of human gingival epithelial cells. The induction of the death induced by short chain fatty acid treatment required reactive oxygen species generation, autophagy induction, and acetylation activity of histone acetyltransferases. In addition, we have constructed 3-demensional culture model which is similar to original gingival tissue.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究の成果は、歯垢が蓄積している状況下での歯肉上皮細胞の細胞死の誘導メカニズムの一端を解明した。これらの細胞死に伴って関節リウマチ発症関連因子や炎症促進因子の放出が起こることから、細胞死誘導情報伝達経路の阻害による関節リウマチ予防法および、歯肉における炎症惹起の予防法を開発できる可能性が大きく高まった。今後の研究の進展により、これまでわかっていなかった歯周病が関与する関節リウマチメカニズムの解明およびその予防法開発が期待できる状況を作ることができたと考える。
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