2016 Fiscal Year Final Research Report
Innovation of diagnosis and treatment for SIRS by intracellular trafficking of CXCR1 and CXCR2 in neutrophils.
Project/Area Number |
26461919
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General surgery
|
Research Institution | Kumamoto University |
Principal Investigator |
Kamohara Hidenobu 熊本大学, 大学院生命科学研究部(医), 准教授 (90398222)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Keywords | neutrophil / CXCL-8 / CXCL-1 / CXCL-2 / SIRS / cellular trafficking / Rab |
Outline of Final Research Achievements |
NeNeutrophils migration is the early process of systemic inflammatory response by SIRS. Curcumin, an inhibitor of NF-kappa B, inhibits neutrophils migration in a dose dependent manner. In this study, it depended on the recovery (recycle) on the surface of CXCR-1/2 which was a receptor of CXCL-8. Its recycling activity of CXCR-1/2 was suppressed by Curcumin. Although the binding of CXCL-8 and CXCR-1/2 was internalized and desensitized in endosome. Rab-11 which was the intracellular transport protein bound to CXCR-1/2. Rab-11 contributed to the recycle regulation of CXCR-1/2. These results suggested that intracellular trafficking molecules could be novel targets in treatment of SIRS.
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Free Research Field |
Critcal Care Medicine
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