| Project/Area Number |
25463225
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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) |
清浦 有祐 奥羽大学, 歯学部, 教授 (90194951)
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| Co-Investigator(Renkei-kenkyūsha) |
MATSUSHITA KENJI 国立研究開発法人国立長寿医療研究センター, 部長 (90253898)
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| Research Collaborator |
MATSUYAMA TAKASHI 鹿児島大学, 大学院医歯学総合研究科, 准教授 (40253900)
SHIMAUCHI HIDETOSHI 東北大学, 大学院歯学研究科, 名誉教授 (70187425)
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥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-33 / 歯肉上皮細胞 / 歯肉上皮バリア破綻 / 口腔粘膜バリア破綻 / 活性型ビタミンD3 / 慢性アレルギー炎症 / 慢性アレルギー性炎症 |
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| Outline of Final Research Achievements |
The cytokine IL-33 is constitutively expressed in epithelial cells and it augments Th2 cytokine-mediated inflammatory responses. We aimed to determine the role of the periodontal pathogen, Porphyromonas gingivalis, in the enhanced expression of IL-33 in human gingival epithelial cells. We detected IL-33 in inflamed gingival epithelium from patients with chronic periodontitis, and found that P. gingivalis increased IL- 33 expression in the cytoplasm of human gingival epithelial cells in vitro. P. gingivalis gingipain-null mutant KDP136 did not induce IL-33 expression. A small interfering RNA for protease-activated receptor-2 (PAR-2) as well as inhibitors of phospholipase C, p38 and NF-κB inhibited the expression of IL-33 induced by P. gingivalis. These results indicate that the PAR-2/IL-33 axis is promoted by P. gingivalis infection in human gingival epithelial cells through a gingipain-dependent mechanism.
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