2018 Fiscal Year Final Research Report
Elucidation of the pathology of maxillofacial analgesia targeting the nerve-immune system of trigeminal ganglion and development of therapeutic method
| Project/Area Number |
17K19772
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Oral Science and related fields
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| Research Institution | Kagoshima University |
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Principal Investigator |
Goto Tetsuya 鹿児島大学, 医歯学域歯学系, 教授 (70253458)
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| Co-Investigator(Kenkyū-buntansha) |
原 博満 鹿児島大学, 医歯学域医学系, 教授 (20392079)
八坂 敏一 鹿児島大学, 医歯学域医学系, 准教授 (20568365)
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| Research Collaborator |
YASAKA Toshiharu 鹿児島大学, 医歯学域医学系, 准教授 (20568365)
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| Project Period (FY) |
2017-06-30 – 2019-03-31
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| Keywords | 三叉神経節 / 神経細胞 / マクロファージ / 神経免疫系 / 神経原性炎症 / 神経ペプチド |
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| Outline of Final Research Achievements |
In order to investigate the interaction between neurons in the trigeminal nerve and cells in the immune system, the maxillary nerve of the mouse was ligated to examine the dynamics of macrophage-like cells in the trigeminal ganglia. After nerve cell injury, an increase in resident Iba-1 labeled macrophage-like cells were observed, and the cell body showed an activated state. The activated macrophage-like cells then migrated to the nerve cells, and squeezed between satellite cells surrounding the nerve cells to contact the nerve cells and eventually to surround the nerve cells. It has been known that neurons in the trigeminal nerve have been involved in neurogenic inflammation, but the neuro-immune system is supposed to exist in the trigeminal ganglion, its function is regulated by the interaction between trigeminal neuron and macrophage-like cells in the immune system.
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| Free Research Field |
口腔組織学
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| Academic Significance and Societal Importance of the Research Achievements |
三叉神経は主に頭頸部の痛覚の伝導に関与するが、一方では三叉神経節内の一次ニューロンはサブスタンスPなどの神経ペプチドを産生し、傷害を受けた部位に逆行性に放出することにより血管透過性等を調節し、炎症のモジュレーターとして働く。今回の研究では、その三叉神経節内の神経細胞の働きが三叉神経節内の免疫系のマクロファージ様細胞によって調節を受けていることを示すものである。これらの結果は体表の障害は末梢の神経節レベルの神経-免疫系システムで対応していることを示すものであり、今後、この防御機構が破綻したアトピー性皮膚炎などの治療法の開発に貢献することが期待される。
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