| Project/Area Number |
23591870
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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 |
General surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KINOSHITA Yoshihiro 熊本大学, 生命科学研究部, 教授 (30195341)
SAGISHIMA Katsuyuki 熊本大学, 医学部附属病院, 助教 (40336235)
HIROSAKO Susumu 熊本大学, 生命科学研究部, 助教 (70432995)
SAKAI Keisuke 熊本大学, 医学部附属病院, 助教 (10433038)
ARAKAWA Hirofumi 独立行政法人国立がん研究センター, 部長 (70313088)
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| Co-Investigator(Renkei-kenkyūsha) |
SHIMOZATO Osamu 千葉県がんセンター, がん治療耐性克服研, 研究員 (30344063)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | SIRS / TRAIL / TRAIL受容体 / 好中球 / ＴＮＦα / ＩＦＮγ / アポトーシス / 実験医学 / 白血球 / 細胞死 / Leukocytes / 分子生物学 / TRAIL receptor |
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| Research Abstract |
We have been identified that neutrophils express TRAIL and TRAIL-R which were induced by IFNgamma and reduced by TNFalpha. Finally, TNFalpha induced the netrophils apoptosis and IFNgamma reduced. In the present study, leukocytes were isolated in peripheral blood and local exudates from post-operative drain in SIRS. The level of TRAIL, TRAIL-R1, and -R2 (death receptor) mRNA were significant higher and the level of TRAIL-R3 and -R4 (decoy receptor) mRNA were significant lower in leukocytes from exudates than leukocytes form peripheral blood. Up- or down-regulation of TRAIL receptor expression by TNFalpha or IFNgamma can affect the susceptibility of neutrophils to TRAIL. In local inflammatory field, neutophils are activated by high amount of cytokines and neutophils expressing TRAIL, -R1 and -R2 can transit to be apoptosis. TRAIL signaling pathway could potentially regulate the fate of tissue-infiltrating neutrophils during SIRS.
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