Activation of M2-type macrophages in the late phase of cerebral ischemia promotes neurogenesis with cleaning of the infarct area.

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K10306
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurosurgery
• Research Institution: Fukuoka University (2016-2017); The University of Tokushima (2015)
• Principal Investigator: Yagi Kenji 福岡大学, 医学部, 講師 (80551837)
• Co-Investigator(Kenkyū-buntansha): 宇都 義浩 徳島大学, 大学院社会産業理工学研究部(生物資源産業学域), 教授 (20304553) ; 永廣 信治 徳島大学, 病院, 病院長 (60145315)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 脳・神経 / 脳梗塞 / Ｍ１/Ｍ２様マクロファージ / 炎症性サイトカイン / phagocytosis / 神経再生

Outline of Final Research Achievements

Brain ischemia promotes the recruitment of various cell types to the brain. Group-specific component protein-derived macrophage activating factor (GcMAF) has various functions including activation of M2-type macrophages and the improvement of motor disability. We tested whether activation of M2-type macrophage by GcMAF after brain ischemia induces beneficial effects. In the early phase of post-ischemia, GcMAF had no beneficial effects. In the late phase, it promoted the clearance of the infarct area; elevated the mRNA level of arginase-1 and increased CD163+ M2-like macrophages in the peri-infarct region. They co-localized with CD36+- and CD68+- but not Iba-1+ cells.. Treatment with GcMAF increased in the incorporation of BrdU and the appearance of NeuN+ and MAP2+ cells in the peri-infarct region mildly improved the neurological deficit. The activation of M2-like macrophages by GcMAF in the late phase may play a therapeutic role.

Free Research Field

脳神経外科学