Are contacts between ganglionic macrophages and neurons a switch for neuropathic pain?

2024 Fiscal Year Final Research Report

• Project/Area Number: 20K09881
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 57010:Oral biological science-related
• Research Institution: Kagoshima University
• Principal Investigator: Iwai Haruki 鹿児島大学, 医歯学域歯学系, 助教 (30452949)
• Co-Investigator(Kenkyū-buntansha): 鈴木 甫 鹿児島大学, 医歯学域歯学系, 助教 (10623340) ; 八坂 敏一 新潟医療福祉大学, 健康科学部, 教授 (20568365) ; 安宅 弘司 神戸薬科大学, 薬学部, 特任助教 (30563358)
• Project Period (FY): 2020-04-01 – 2025-03-31
• Keywords: マクロファージ / キメラマウス / 末梢神経損傷 / 感覚神経節 / 神経炎症 / M1 / M2

Outline of Final Research Achievements

After nerve injury, the number of both bone-marrow-derived and tissue-resident macrophages increased in sensory ganglia. However, most macrophages that increased in sensory ganglia were found to be tissue-resident. After nerve injury, macrophages in sensory ganglia entered between primary neurons and satellite cells, forming contact-like structures between macrophages and neurons. Furthermore, these contact-like structures were confirmed by electron microscopy to involve direct contact between macrophages and neurons. These macrophages that arise after nerve injury were found to be CD206 phenotype.

Free Research Field

神経解剖学

Academic Significance and Societal Importance of the Research Achievements

慢性疼痛は、世界的な有病率の高さと医療費および生産性の損失という観点から、身体的および経済的な面で人々に多大な影響を与えている。この中に含まれる神経因性疼痛は、一般の鎮痛薬ではほとんど改善が期待できないことから、その原因究明と有効な治療法の開発が望まれている。本研究は、このような神経因性疼痛の発症機序の解明に寄与するだけでなく、治療法の開発に繋がることが期待される。