| Project/Area Number |
23792692
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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 |
Community health/Gerontological nurisng
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| Research Institution | The University of Tokyo |
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Principal Investigator |
NAKAGAMI Gojiro 東京大学, 大学院・医学系研究科, 講師 (70547827)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | クオラムセンシング / シグナル伝達 / 褥瘡 / 感染 / 緑膿菌 / 創傷看護学 / トランスレーショナルリサーチ / バイオエンジニアリングナーシング / マトリックスメタロプロテイナーゼ / 感染看護 / 分子生物学 / 遺伝子発現 / MMP / AP-1 |
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| Research Abstract |
This study aimed to establish an appropriate strategy for prevention and control of pressure ulcer infection, an unsolved problem among elderly population. For exploring mechanism responsible for pressure ulcer infection, we targeted Pseudomonas aeruginosa quorum sensing system. We demonstrated the increased expression of matrix metalloproteinase (Mmp-9) gene, which acts as an inflammatory cytokine and proteinase, in fibroblasts exposed to 3-oxo-dodecanoyl homoserine lactone (AHL). This induction was occurred via AP-1/ERK/p38 signaling pathway. For further exploring mechanism above this pathway, we assessed the gene expression changes by DNA microarray using fibroblast exposed to 10μM of AHL, which is determined to be detrimental concentration for fibroblast response to AHL. This study suggested the contribution of AHL on the inflammation and tissue destruction by P. aeruginosa during wound healing process through the specific signaling pathway to fibroblast by inducing Mmp-9 gene expression.
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