| Project/Area Number |
16K20437
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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 |
Pathobiological dentistry/Dental radiology
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| Research Institution | Hiroshima University |
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Principal Investigator |
Furusho Hisako 広島大学, 医歯薬保健学研究科(歯), 助教 (00634461)
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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: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | red complex / TLR2 / NASH / 歯性感染 / Red complex / 炎症 |
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| Outline of Final Research Achievements |
In vivo experiment, crown-like structure (CLS) number and fibrosis were increased in high-fat-diet induced wild type mice groups (WT-HFD), excluding 1 group, and they were decreased in high-fat-diet induced TLR2 (TLR2KO-HFD) groups ultimately. Similarly, IL-1β mRNA expression, upregulated in WT-HFD groups, were restrained in TLR2KO-HFD groups. In vitro experiment, IL-1β and IL-6 mRNA expression were upregulated in the steatotic hepatocyte, stimulated by each red complex (Pg, Td, Tf) dead body stimulation. After the dosage of the TLR2 inhibitor, the mRNA upregulation were suppressed. It was revealed that the TLR2 pathway participated in NASH progression by the red complex odontogenic infection.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は顎骨における歯周病原細菌感染と肝疾患の関連性を課題としている。今回の研究において作成する歯性感染モデルでは、歯周病原細菌の中のred complexを使用し、各菌単独およびその組み合わせにおいてより患者の病態を模倣したnaturalな状態を観察している。red complex歯性感染によるNASH病態増悪の機序についてTLR2の役割を明らかにしたことは、脂肪肝患者におけるTLR2を標的とした新たな治療法開発につながり、社会に還元できる有意義な研究であると考える。
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