2017 Fiscal Year Final Research Report
The analysis of mechanism in the serious inflammatory responses induced by dead cells as aging.
| Project/Area Number |
15K07949
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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 | Toho University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
小林 芳郎 東邦大学, 理学部, 教授 (10134610)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | 老化 / アポトーシス / 炎症 / マクロファージ / 死細胞 |
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| Outline of Final Research Achievements |
We investigated why inflammatory responses was increased in aged mice upon injection of dead cells and why the phagocytic capacity of peritoneal resident macrophages from aged mice was reduced. When cocultured with dead cells, the peritoneal resident macrophages from aged mice significantly produced MIP-2, whereas MIP-2 production by macrophages from WT young mice required IFN-γ. The peritoneal resident macrophages from aged mice expressed CD40, a M1 macrophage marker, as in the case of M1 macrophages. Furthermore, M1 macrophages exhibited less phagocytic capacity as to dead cells than non-treated macrophages. These results suggest that the phenotype of peritoneal resident macrophages is skewed toward M1-like in aged mice and that such skewing toward M1-like is involved in enhancement of inflammatory responses induced by dead cells in aged mice.
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| Free Research Field |
免疫
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