| Project/Area Number |
15H04766
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pain science
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| Research Institution | Kagoshima University (2016-2017)
Saga University (2015) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
村田 祐造 佐賀大学, 医学部, 准教授 (20128143)
原 博満 鹿児島大学, 医歯学域医学系, 教授 (20392079)
吉田 裕樹 佐賀大学, 医学部, 教授 (40260715)
山崎 晶 九州大学, 生体防御医学研究所, 教授 (40312946)
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| Co-Investigator(Renkei-kenkyūsha) |
TSUDA Makoto 九州大学, 薬学研究院, 教授 (40373394)
KAWAI Taro 奈良先端科学技術大学院大学, 先端科学技術研究科, 教授 (50456935)
HIRAKAWA Naomi 佐賀大学, 医学部, 准教授 (20173221)
SONOHATA Motoki 佐賀大学, 医学部, 准教授 (50304895)
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| Research Collaborator |
IIZASA Ei'ichi 鹿児島大学, 医歯学域医学系, 助教 (20631998)
SASAGURI Tomoko 佐賀大学, 医学部, 助教 (00380767)
ISHIKAWA Asako 佐賀大学, 医学部, 助教 (90404128)
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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 |
¥18,330,000 (Direct Cost: ¥14,100,000、Indirect Cost: ¥4,230,000)
Fiscal Year 2017: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2016: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2015: ¥11,830,000 (Direct Cost: ¥9,100,000、Indirect Cost: ¥2,730,000)
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| Keywords | 神経障害性疼痛 / パターン認識受容体 / 神経免疫連関 / 疼痛学 / 脳内炎症 / 神経障害性痛 |
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| Outline of Final Research Achievements |
Neuropathic pain is a type of chronic pain that usually does not respond to non-steroidal anti-inflammatory drugs and opioids. Thus, better treatments for this condition are eagerly sought. Neuropathic pain result from damage to the nervous system. Molecules released from damaged cells are called damage-associated molecular patterns and are able to trigger pathogenesis of this disease through stimulating pattern recognition receptors (PRRs). In this study, we investigated roles of PRRs on the pathogenesis of neuropathic pain. Mice lacking a certain PRR showed impaired pain hypersensitivity after peripheral nerve injury. Cells that expressed the receptor were identified as infiltrating leucocytes in injured nerve. These results suggest that the PRR investigated here contribute the pathogenesis of neuropathic pain.
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