2017 Fiscal Year Final Research Report
The effect of AIM for periodontitis and body
| Project/Area Number |
15K20624
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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 |
Periodontology
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| Research Institution | Kyushu Dental College |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
Nakamichi Ikuo 九州歯科大学, 健康増進学講座総合内科学講座, 講師 (60419570)
Nakashima Keisuke 九州歯科大学, 口腔機能学講座歯周病学分野, 教授 (80227785)
Obara Shigeyuki 九州歯科大学, 口腔機能学講座歯周病学分野, 特別研修員 (70735878)
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| Research Collaborator |
Nishihara Tatsuji 九州歯科大学, 健康増進学講座感染分子生物学分野, 教授 (80192251)
Ariyoshi Wataru 九州歯科大学, 健康増進学講座感染分子生物学分野, 准教授 (40405551)
Okinaga Toshinori 九州歯科大学, 健康増進学講座感染分子生物学分野, 講師 (60582773)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | AIM / 慢性歯周炎 / 動脈硬化 |
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| Outline of Final Research Achievements |
Macrophage made an apoptosis inhibitor of macrophage (AIM) in the atherosclerotic plaque. AIM that was produced from periodontal tissue in periodontitis has the possible of potential clinical maker detecting periodontitis and inducing factor for atherosclerosis. The purpose of this research is to determine a role for AIM in periodontitis. Inflammation inhibited a cell adhesion in HUVEC. It induced that monocytes in blood recruited into an intima of a blood vessel. In addition, it made a foam cell formation in intima.
Recent studies revealed that IL-17A was secreted from Th17 cells in this process related an expression of cell adhesion factors. We focused on a role of IL-17A in this research.
The result indicated that IL-17A induced increasing an expression of cell adhesion factors in HUVEC and monocytes, and induced developing atherosclerosis.
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| Free Research Field |
歯周病学
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