We quantitatively investigated temporal changes of macrophages and microglia (MΦ/MG) after focal infarction of the internal capsule using a macaque model we recently established. Immunoreactivity for Iba1, a general marker for MΦ/MG, in the periinfarct core gradually increased from 0 days to 2–3 weeks after infarction, and the increased immunoreactivity continued at least until 6 months; no study in rodents has reported increased Iba1-immunoreactive cells for so long. Retrograde atrophy or degeneration of neurons in layer V of the primary motor cortex, where the descending motor tract originates, was seen as secondary damage. Here we found that Iba1-positive MΦ/MG transiently increased in layer V during several weeks after the infarction. Therefore, the time course of MΦ/MG activation differs between the perilesional area and the remote brain area where secondary damage occurs to tissue initially preserved after the infarct. Detailed analyses using the functional phenotype markers CD68, CD86, and CD206, as well as cytokines released by cells with each phenotype, suggest an anti-inflammatory role for activated MΦ/MG both in the periinfarct core during the chronic phase and in the primary motor cortex.

我们使用我们最近建立的猕​​猴模型定量研究了内囊局灶性梗塞后巨噬细胞和小胶质细胞 (MΦ/MG) 的时间变化。Iba1（MΦ/MG 的一般标志物）在梗塞周围核心的免疫反应性从 0 天到梗塞后 2-3 周逐渐增加，并且免疫反应性增加至少持续到 6 个月；长期以来，没有任何啮齿类动物研究报告 Iba1 免疫反应细胞增加。下行运动束起源的初级运动皮层 V 层神经元的逆行萎缩或退化被视为继发性损伤。在这里，我们发现 Iba1 阳性 MΦ/MG 在梗塞后数周内在 V 层中瞬时增加。所以，MΦ/MG 激活的时间过程在病灶周围区域和远端脑区域之间不同，在这些区域，梗塞后最初保存的组织发生继发性损伤。使用功能表型标记 CD68、CD86 和 CD206 以及每种表型细胞释放的细胞因子进行的详细分析表明，活化的 MΦ/MG 在慢性期梗塞周围核心和初级运动中均具有抗炎作用皮质。