| Project/Area Number |
16K20418
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Fukuoka Dental College |
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Principal Investigator |
NARITA Yuka 福岡歯科大学, 口腔歯学部, 助教 (50758050)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 歯周病原細菌 / 獲得免疫 / 病原細菌 / 歯学 / 微生物 / 免疫学 |
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| Outline of Final Research Achievements |
Periodontal disease is a chronic inflammatory disease caused by oral pathogenic bacteria, and immune response contributes to their onset and progression. The red complex, Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola, are most important pathogens in severe periodontitis and co-aggregate with each other for their survival effectively. The immunoresponse of Th17 cells contributes to its clinical condition in periodontitis. Therefore, we conducted a comprehensive analysis how 3 species of the red complex affected T helper cell differentiation. In this study, we identified several cell components of the red complex to induce Th17 differentiation.
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| Academic Significance and Societal Importance of the Research Achievements |
歯周病は国民の多くが罹患する慢性疾患であるが、この口腔疾患が糖尿病などの全身疾患と相互に影響しうる。本研究では、重度の歯周病患者に特徴的に見られる歯周病原細菌に着目し、歯周病病態形成に関わる宿主のヘルパーT細胞Th17を誘導する歯周病原細菌由来の抗原を探索した。微生物と宿主の両側から歯周病発症のメカニズムを明らかにすることで、この成果を将来歯周病ワクチンなどの予防や治療分野に応用可能である。
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