2021 Fiscal Year Final Research Report
Next step in the oral-gut connection: Do swallowed periodontopathogenic bacteria exacerbate colitis?
Project/Area Number |
19K10126
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 57030:Conservative dentistry-related
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Research Institution | Niigata University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
多部田 康一 新潟大学, 医歯学系, 教授 (20401763)
片倉 響子 福島県立医科大学, 医学部, 講師 (70423788)
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Project Period (FY) |
2019-04-01 – 2022-03-31
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Keywords | ペリオドンタルメディスン / 歯周病 / 実験的腸炎モデルマウス / 上皮バリア / P. gingivalis |
Outline of Final Research Achievements |
This study aimed to evaluate the effects of ingested periodontal pathogens on experimental colitis in mice and to elucidate its underlying mechanisms. We found that the oral administration of P. gingivalis significantly increased the severity of colitis when compared to other pathogens in the DSS-induced colitis model. The ingested P. gingivalis disrupted the colonic epithelial barrier by decreasing the expression of tight junction proteins in vivo. In vitro permeability assays using the intestinal epithelial cell line suggested the P. gingivalis-specific epithelial barrier disruption. The possible involvement of gingipains in the exacerbation of colitis was implied by using P. gingivalis lacking gingipains.
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Free Research Field |
歯周病学
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Academic Significance and Societal Importance of the Research Achievements |
今回の薬剤誘導性実験的腸炎モデルマウスを用いた一連の研究において、経口投与されたP. gingivalisが腸管上皮バリア機能の破綻を介して腸炎重症化に関与することが確認されたことから、歯周炎が炎症性腸疾患に悪影響を与えることが示唆された。そのメカニズムのひとつとして、P. gingivalis由来のプロテアーゼgingipainの関与が示唆されたことから、炎症性腸疾患の重症化予防や治療におけるプロテアーゼ阻害薬を用いた創薬が期待される。
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