2018 Fiscal Year Final Research Report
The destructive mechanisms of epihthelial barrier funtion by peirodontal bacteria in membrane traffic
| Project/Area Number |
17K17083
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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 | Osaka University |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Keywords | 分子生物学 / 組織工学 / 細菌学 / 歯周病 / Porphyromonas gingivalis |
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| Outline of Final Research Achievements |
Porphyromonas gingivalis is a major pathogen in severe and chronic manifestations of periodontal disease, which is one of the most common infections of humans. A central feature of P. gingivalis pathogenicity is dysregulation of innate immunity at the gingival epithelial interface; howerver, the molecular basis for the P. gingivalis-dependent abrogation of epithelial barrier function remains undetermined. Gingival epithelial cells express JAM1, a tight junction-associated protein, regulates epithelial barrier function. Here we show that the Arg-specific or Lys-specific cysteine proteases (gingipains) secreted by P. gingivalis can specifically degrade JAM1. A P. gingivalis lacking gingipains was impaired in degradation of JAM1. Specific degradation of JAM1 by P. gingivalis provides the molecular basis for a bacterial strategy leading to periodontitis.
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| Free Research Field |
予防歯科学
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| Academic Significance and Societal Importance of the Research Achievements |
日本国における歯周病患者の割合は増加しているが，歯周病の病因論には不明な点が多い．歯周病菌Porphyromonas gingivalis が特異的に分解する上皮バリア関連タンパク質を明らかにすることは，歯周病の発症機序を分子生物学的に調べることを可能とする．また，歯肉上皮組織の作成法を確立することは，歯周病の未病の段階でのヒト生体組織の形態学的解析を可能とする．さらに，歯周病の宿主要因を遺伝学的に調べることを可能とする．P. gingivalis の感染機構を明らかにすることは，本菌の宿主への長期感染を制御できる可能性がある．
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