Analysis of mechanism for pro-inflammatory and anti-inflammatory balance and role of Th17 cells in pulpitis
| Project/Area Number |
15K11115
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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 |
Conservative dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
NAKANISHI Tadashi 徳島大学, 大学院医歯薬学研究部(歯学系), 准教授 (00217770)
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| Co-Investigator(Kenkyū-buntansha) |
湯本 浩通 徳島大学, 大学院医歯薬学研究部(歯学系), 教授 (60284303)
細川 義隆 徳島大学, 病院, 講師 (90346601)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 歯髄炎 / 象牙芽細胞 / Th17 / 歯髄 / 炎症 / サイトカイン / IL-17 / ケモカイン |
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| Outline of Final Research Achievements |
The purpose of this study was to elucidate the role of Th17 cells in the pathogenesis of pulpitis, and thus we examined the effect of interleukin(IL)-17 on CCL20 production from KN-3 cells established as rat odontoblast-like cells.
IL-17 increased CCL-20 production from KN-3 cells exposed to IL-1. The treatment of IL-17 also enhanced the phosphorylation of mitogen-activated protein kinases (MAPKs) in IL-1 stimulated KN-3 cells. Moreover, epigallocatechin-3 gallate, a representative type of catechins, reduced CCL20 production from activated KN-3 cells.
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Report
(4 results)
Research Products
(3 results)
