| Project/Area Number |
15K19492
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurology
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 神経因性疼痛 / ミクログリア / アストログリア / 気管支喘息 / アトピー性皮膚炎 / エンドセリン / 神経障害性疼痛 / 脊髄炎 / アロディニア / アストロサイト |
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| Outline of Final Research Achievements |
We studied whether allergic/atopic inflammation affects the spinal nociceptive system. We found that mice with atopy had widespread activation of microglia and astroglia in the spinal cord than those without atopy, and displayed neuropathic pain. Microarray analysis of isolated microglia revealed marked upregulation of endothelin receptor type B (EDNRB) in atopic mice. EDNRB expression was enhanced in microglia and astroglia while endothelin-1, an EDNRB ligand, was increased in serum, lungs, and epidermis of atopic mice. The EDNRB antagonist BQ788 abolished glial activation and allodynia. We found increased serum endothelin-1 and activation of spinal microglia and astroglia with EDNRB upregulation in atopic patients with neuropathic pain. Therefore, allergic/atopic inflammation induces diffuse glial activation, influencing the nociceptive system via the EDNRB pathway.
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