| Project/Area Number |
16K11477
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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 |
Functional basic dentistry
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| Research Institution | Nihon University (2019)
Kyushu University (2016-2018) |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | カテプシンE / 好中球 / 一次求心性神経 / 慢性疼痛 / 機械的アロディニア / 神経障害性疼痛 / ヒト乳歯歯髄幹細胞 / 歯髄幹細胞 / 脊髄後根神経節 |
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| Outline of Final Research Achievements |
The effects of dental pulp stem cells on chronic pain was found to be suppression of immune cells accumulating in the cell bodies of primary afferent fibers which transmit nociceptive information from the peripheral tissue to the spinal dorsal horn. Neutrophils were accumulated in response to induction of chemokine (C-X-C motif) ligand 1 (CXCL1), a kind of chemokine, in dorsal root ganglion neurons. Adoptive transferred activated wild-type but not cathepsin E-deficient neutrophils elicited mechanical allodynia in naive mice. Pro-elastase was cleaved within neutrophils in a cathepsin E-dependent manner. Elastase released from neutrophils could cause facilitation of neuronal activity via protease activated receptor 2. Activation of neutrophils was mediated through toll-like receptor 4.
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| Academic Significance and Societal Importance of the Research Achievements |
神経障害性疼痛は既存の鎮痛薬ですら効果が乏しい症状である。そのため，新たな鎮痛薬開発が望まれている。多くの研究が行われているにも関わらず，神経障害性疼痛のメカニズムおよび治療法は未だ十分に明らかにされていない。このような中，神経障害性疼痛の治療方法としての幹細胞の意義を提示することができた。また，免疫細胞を介したメカニズムも明らかにすることができた。これらの情報を基に，今後新たな治療方法の開発への応用に繋げることができる可能性を提示できたと考える。
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