Porphyromonas gingivalis induces the production of IL-31 by human mast cells, resulting in dysfunction of the gingival epithelial barrier
| Project/Area Number |
16K11824
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Periodontology
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| Research Institution | Tohoku University |
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Principal Investigator |
Tada Hiroyuki 東北大学, 歯学研究科, 講師 (70431632)
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| Co-Investigator(Kenkyū-buntansha) |
西岡 貴志 東北大学, 歯学研究科, 助教 (50641875)
松下 健二 国立研究開発法人国立長寿医療研究センター, 口腔疾患研究部, 部長 (90253898)
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| Project Period (FY) |
2016-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 慢性歯周炎 / Porphyromonas gingivalis / Interleukin-31 / 歯肉上皮細胞 / 歯肉上皮バリア破綻 / マスト細胞 / 口腔粘膜バリア破綻 / 歯周病原細菌 / バリア破綻 / 歯周病態・診断学 |
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| Outline of Final Research Achievements |
Interleukin (IL)-31 participates in the pathogenesis of chronic inflammatory diseases. We investigated the contribution of mast cells to the induction of IL-31 production following infection with the periodontal pathogen, Porphyromonas gingivalis. We found that oral infection with P. gingivalis increased IL-31 expression in the gingival tissues of mice. The P. gingivalis-induced IL-31 production by human mast cells was dependent on the P. gingivalis lysine-specific protease gingipain-K. Notably, the P. gingivalis-induced IL-31 production by mast cells led to the downregulation of claudin-1, a tight junction molecule, in gingival epithelial cells, resulting in an IL-31-dependent increase in the paracellular permeability of the gingival epithelial barrier. These findings suggest that IL-31 produced by mast cells in response to P. gingivalis infection causes gingival epithelial barrier dysfunction, which may contribute to the chronic inflammation observed in periodontitis.
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| Academic Significance and Societal Importance of the Research Achievements |
歯周病は、歯周病原細菌による慢性炎症を特徴とする感染症です。慢性炎症が長く続くと歯の周りの組織は破壊され、歯の喪失に至ります。本研究は、歯周病原細菌の感染によりヒトマスト細胞からインターロイキン-31という炎症物質が産生されることを発見しました。インターロイキン-31は歯ぐきの粘膜を維持する粘膜バリアを破壊し、歯周病原細菌の感染を悪化させることを発見しました。歯肉粘膜バリアの破綻は、歯周炎の慢性化に関わる可能性が想定されます。今後、歯周病における慢性炎症のコントロールを目的とした予防・治療への展開が期待されます。
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Report
(5 results)
Research Products
(30 results)
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[Journal Article] Dectin-2-Mediated Signaling Leads to Delayed Skin Wound Healing through Enhanced Neutrophilic Inflammatory Response and Neutrophil Extracellular Trap Formation.2019
Author(s)
Miura T, Kawakami K, Kanno E, Tanno H, Tada H, Sato N, Masaki A, Yokoyama R, Kawamura K, Kitai Y, Takagi N, Yamaguchi K, Yamaguchi N, Kyo Y, Ishii K, Imai Y, Saijo S, Iwakura Y, Tachi M.
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Journal Title
J Invest Dermatol
Volume: 139(3)
Issue: 3
Pages: 702-711
DOI
Related Report
Peer Reviewed / Int'l Joint Research
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[Journal Article] Periodontitis induced by bacterial infection exacerbates features of Alzheimer's disease in transgenic mice2017
Author(s)
Ishida N, Ishihara Y, Ishida K, Tada H, Funaki-Kato Y, Hagiwara M, Ferdous T, Abdullah M, Mitani A, Michikawa M, Matsushita K.
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Journal Title
NPJ Aging Mech. Dis.
Volume: 3
Issue: 1
Pages: 15-15
DOI
NAID
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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