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2014 Fiscal Year Final Research Report

The effect of aging on dead cells induced inflamatory responses and analysis of its mechanisms

Research Project

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Project/Area Number 24590100
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Biological pharmacy
Research InstitutionToho University

Principal Investigator

NAGATA Kisaburo  東邦大学, 理学部, 准教授 (10291155)

Co-Investigator(Kenkyū-buntansha) KOBAYSHI Yoshiro  東邦大学, 理学部, 教授 (10134610)
Project Period (FY) 2012-04-01 – 2015-03-31
Keywords老化 / 炎症 / アポトーシス / 貪食
Outline of Final Research Achievements

We investigated phagocytosis of late apoptotic cells by peritoneal resident macrophages and infiltration of neutrophil and production of MIP-2 when injected late apoptotic cells to peritoneal cavity. Phagocytosis of apoptotic cells by macrophages from aged mice was significantly lower than that by macrophages from young mice. Upon peritoneal injection of apoptotic cells, the peak time of neutrophil infiltration was earlier and the neutrophil number was greater in aged mice than in young mice. Macrophages from young mice produced MIP-2 in the presence but not the absence of IFN-γ upon phagocytosis of late apoptotic cells. These results suggested that peritoneal resident macrophages in WT aged and SMP30-/-mice might be pre-activated. The present data suggested that resident macrophages are pre-activated and phenotypically changed in WT aged and SMP30-/-mice, causing delayed clearance of apoptotic cells and subsequently rapid and strong inflammation.

Free Research Field

免疫

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Published: 2016-06-03  

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