| Project/Area Number |
15K08416
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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 |
Experimental pathology
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
KOBAYASHI Hiroya 旭川医科大学, 医学部, 教授 (90280867)
OHKURI Takayuki 旭川医科大学, 医学部, 講師 (70564061)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 樹状細胞 / 神経ペプチド / 神経ペプチド受容体 / サイトカイン産生 / 抗原提示能 / 抗原特異的T細胞 / 感染症 / がん |
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| Outline of Final Research Achievements |
In this study, we investigated the precise roles of neuropeptide signaling through NK2R, a receptor of neurokinin A, in tumorigenesis of cancer cells and inflammatory bowel disease (IBD) involving with inflammation and immune responses. We found that NK2R expression levels of murine and human dendritic cells were augmented by type-1 IFN stimulations in a STAT-1-dependent manner. Antigen-specific T cell responses were attenuated in the presence of a NK2R antagonist in vitro. Next, we revealed that in vivo administration of a NK2R antagonist reduced tumorigenesis of CT26 cancer cells and disease state of dextran sulfate sodium (DSS)-induced colitis model. Furthermore, we confirmed that NK2R was expressed in lesion and inflammation areas of patients with hepatocellular carcinoma, cervical cancer, colorectal cancers, and IBD. Based on these findings we speculate that regulation of neuropeptide signaling may be a promising tool in the development of effective therapy for cancers and IBD.
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