| Project/Area Number |
26463136
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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 | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
武富 孝治 久留米大学, 医学部, 助教 (10553290)
西村 英紀 九州大学, 歯学研究院, 教授 (80208222)
福田 隆男 九州大学, 歯学研究院, 助教 (80507781)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | Spry2 / M2 macrophage / efferocytosis / P. gingivalis LPS / IFN-γ / periodontal regeneration / P. gingivalis LPS / Sprouty2 |
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| Outline of Final Research Achievements |
Periodontitis is a chronic inflammatory disorder caused by specific bacteria residing in the biofilm, particularly P gingivalis (Pg). In this study, we investigated the mechanisms through which Spry2 depletion by IFNγ and Pg LPS stimulation affected the physiology of macrophages in vitro. Transfection of macrophages with Spry2 siRNA promoted the expression of genes characteristic of M2 macrophages, IL-10 expression, and enhanced arginase activity, even in cells stimulated with IFNγ and Pg LPS. In addition, we found that PI3K and AKT activation by Spry2 downregulation enhanced efferocytosis of apoptotic cells by increasing Rac1 activation and decreasing NFκB p65 phosphorylation. Collectively, our results suggested that topical administration of Spry2 inhibitors may efficiently resolve inflammation in periodontal disease as macrophage-based anti-inflammatory immunotherapy and may create a suitable environment for periodontal wound healing.
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