Regulation of inflammation, immunity, and tissue repairing by nervous system.
| Project/Area Number |
15K07938
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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 |
Biological pharmacy
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| Research Institution | Health Sciences University of Hokkaido |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
平出 幸子 北海道医療大学, 薬学部, 助教 (50709277)
飯塚 健治 北海道医療大学, 薬学部, 教授 (10344467)
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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 |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ストレス / アドレナリン / 糖質コルチコイド / マクロファージ / TGF-β / 組織修復 |
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| Outline of Final Research Achievements |
Stress events activate the sympathetic nervous system and result in the secretion of catecholamines including adrenaline. In the present study, we examined the influence of the stress-related mediators such as adrenaline and glucocorticoids in inflammation, immunity, and tissue repairing. TGF-b is a multifunctional cytokine responsible for not only immune regulations but also tissue repairing. We found that treatment with adrenaline markedly increased the mRNA expression of TGF-b3 but not TGF-b1 and -b2 in macrophages. In addition, we found that simultaneous treatment with adrenaline and dexamethasone increases cell surface expression of the costimulatory molecule CD86, while decreasing that of the immune checkpoint protein PD-L1 in RAW264.7 macrophages. Further elucidation of the complex pathways regulated by stress-related mediators may lead to the development of a new therapeutic strategies focused on pathogenic immune-response and tissue repair in stress-related disorders.
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Report
(4 results)
Research Products
(13 results)
