| Project/Area Number |
18K17051
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 57030:Conservative dentistry-related
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| Research Institution | The University of Tokushima |
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Principal Investigator |
IKUTA Takahisa 徳島大学, 大学院医歯薬学研究部(歯学域), 助教 (00746563)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 糖尿病関連歯周炎 / 最終糖化産物 / LPS / 低酸素環境 / リポカリン２ / 糖尿病性歯周炎 |
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| Outline of Final Research Achievements |
The effects of advanced glycation end-products (AGEs) and lipopolysaccharide (LPS) the pathological condition of diabetes-associated periodontitis under hypoxia. Hypoxia decreased the expressions of lipocalin 2 (LCN2) and IL-6 in oral epithelial cells. AGEs increased LCN2 and IL-6 expressions, however, LPS did not show any effects. The phosphorylation of MAPK and NF-κB in signal transduction pathway were complicatedly influenced by AGEs and a hypoxia. AGEs-induced LCN2 in epithelial cells promoted a migration of neutrophils and reduced its IL-6 expression. LCN2 is induced by AGEs in oral epithelial cells and may complicatedly influence the formation of pathological conditions of diabetes-associated periodontitis.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は糖尿病関連歯周炎の病態研究に関して，従来から行われてきたLPSやAGEsによる炎症性サイトカイン発現への検討だけでなく，低酸素環境にある歯周ポケット内での反応性やこれまでに調べられていない炎症反応関連因子のリポカリン２(LCN2)による糖尿病関連歯周炎への関与について検討を行った。この結果，低酸素環境は，炎症関連因子や歯周組織細胞に関連する因子の発現やシグナル伝達機構に対して非常に複雑な影響を与えることが判明した。また，口腔上皮細胞由来のLCN2は，好中球の炎症反応に対して複雑な作用を示すことが分かった。今後それぞれの因子や経路に関してさらに詳細な検討が必要となることが示唆された。
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