| Project/Area Number |
17K09674
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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 |
Respiratory organ internal medicine
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
荒屋 潤 東京慈恵会医科大学, 医学部, 教授 (90468679)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 樹状細胞 / オードファジー / COPD / Parkin / オートファジー / 慢性閉塞性肺疾患 |
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| Outline of Final Research Achievements |
Dendritic cells (DC) are though to be important for the introducing inflammatory cells and fibrotic changes in the lung of COPD patients. We aimed to elucidate that autophagy activity inside DC might control the migration of Th1, Th17 and neutrophils into the lung. By examining the lung sample of COPD patients, ubiquitin and p62 expressions inside DC are more pronounce in COPD patients than normal patients, suggesting attenuated activity of autophagy inside DC. In vitro experiment, DC were differentiated from bone marrow by GM-CSF, and Cigarette smoke extract stimulations made DCs from WT mouse to produce more cytokines than Parkin knockout mouse- derived BMDC when LPS was added.
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| Academic Significance and Societal Importance of the Research Achievements |
マウスの骨髄からGM-CSFでBMDCが誘導されることを確認した。このBMDCを使用した結果、サイトカインの分泌は、CSE刺激群でより多く出る傾向が見られたが、Parkinノックアウトマウスから誘導したDCからは、サイトカインは抑制される傾向が見られた。DC内のマイトファジーの低下がサイトカインの分泌抑制に関与している可能性が示唆された。
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