2020 Fiscal Year Final Research Report
Inhibition of intestinal epithelial fucosylation by periodontopathogenic bacteria exacerbates rheumatoid arthritis
Project/Area Number |
19K24073
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Research Category |
Grant-in-Aid for Research Activity Start-up
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Allocation Type | Multi-year Fund |
Review Section |
0907:Oral science and related fields
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Research Institution | Hiroshima University |
Principal Investigator |
Hamamoto Yuta 広島大学, 病院(歯), 歯科診療医 (00848476)
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Project Period (FY) |
2019-08-30 – 2021-03-31
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Keywords | 歯周病 / 関節リウマチ / 腸内細菌叢の変化 |
Outline of Final Research Achievements |
Previous reports have demonstrated that arthritis was exacerbated by orally infection with periodontopathogenic bacteria (Porphyromonas gingivalis, Pg) in RA mice model. In this study, we found that the Pg-infected mice showed altered intestinal microflora, increased inflammatory cytokines in intestinal tissues, and increased citrullinated protein (CP), which is responsible for the production of autoantibodies in RA. Furthermore, fecal microbiota transplantation from Pg-infected mice into a new RA mice model reproduced the same intestinal microbiota and inflammatory changes as Pg-infected group in recipient mice. These results suggest that the changes in the intestinal microbiota caused by Pg infection lead to inflammatory changes and increased CP production in the intestine, which may serve as a scaffold for the production of autoantibodies prior to the onset of RA.
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Free Research Field |
歯周治療学
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Academic Significance and Societal Importance of the Research Achievements |
RAは、発症に先立たって自己抗体が産生されることがわかっており、その環境因子として、喫煙による肺組織の炎症や歯周病によるが歯周組織の炎症がこれまでに報告されている。今回の研究で、歯周病原細菌の感染により腸内細菌叢の変化、腸組織中の炎症性変化とRAの自己抗体産生の原因となるCPの産生亢進が認められた。つまり歯周病原細菌の感染による腸内環境の変化が、RAの自己抗体産生の足場となっており、新規の環境因子である可能性が示唆された。 RAと歯周炎の好発年齢は類似しており、早期からの歯科介入による歯周病予防や治療が、RAの発症や病状悪化を予防することに対して非常に有効である可能性が示唆された。
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