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首页> 外文期刊>Journal of neuroinflammation >Intravenous multipotent adult progenitor cell therapy after traumatic brain injury: modulation of the resident microglia population
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Intravenous multipotent adult progenitor cell therapy after traumatic brain injury: modulation of the resident microglia population

机译：脑外伤后静脉内多能成年祖细胞疗法：驻地小胶质细胞群体的调节。

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Introduction We have demonstrated previously that the intravenous delivery of multipotent adult progenitor cells (MAPC) after traumatic brain injury affords neuroprotection via interaction with splenocytes, leading to an increase in systemic anti-inflammatory cytokines. We hypothesize that the observed modulation of the systemic inflammatory milieu is related to T regulatory cells and a subsequent increase in the locoregional neuroprotective M2 macrophage population. Methods C57B6 mice were injected with intravenous MAPC 2 and 24 hours after controlled cortical impact injury. Animals were euthanized 24, 48, 72, and 120 hours after injury. In vivo, the proportion of CD4+/CD25+/FOXP3+ T-regulatory cells were measured in the splenocyte population and plasma. In addition, the brain CD86+ M1 and CD206+ M2 macrophage populations were quantified. A series of in vitro co-cultures were completed to investigate the need for direct MAPC:splenocyte contact as well as the effect of MAPC therapy on M1 and M2 macrophage subtype apoptosis and proliferation. Results Significant increases in the splenocyte and plasma T regulatory cell populations were observed with MAPC therapy at 24 and 48 hours, respectively. In addition, MAPC therapy was associated with an increase in the brain M2/M1 macrophage ratio at 24, 48 and 120 hours after cortical injury. In vitro cultures of activated microglia with supernatant derived from MAPC:splenocyte co-cultures also demonstrated an increase in the M2/M1 ratio. The observed changes were secondary to an increase in M1 macrophage apoptosis. Conclusions The data show that the intravenous delivery of MAPC after cortical injury results in increases in T regulatory cells in splenocytes and plasma with a concordant increase in the locoregional M2/M1 macrophage ratio. Direct contact between the MAPC and splenocytes is required to modulate activated microglia, adding further evidence to the central role of the spleen in MAPC-mediated neuroprotection.
机译：引言我们之前已经证明，颅脑外伤后多能成年祖细胞（MAPC）的静脉内递送通过与脾细胞的相互作用提供神经保护作用，从而导致全身性抗炎细胞因子的增加。我们假设观察到的系统性炎症环境的调节与T调节细胞和局部神经保护性M2巨噬细胞种群的随后增加有关。方法在C57B6小鼠皮层撞击伤发生后2和24小时内静脉注射MAPC。受伤后24、48、72和120小时对动物实施安乐死。在体内，在脾细胞群和血浆中测量了CD4 + / CD25 + / FOXP3 + T调节细胞的比例。另外，对脑CD86 + M1和CD206 + M2巨噬细胞群体进行了定量。完成了一系列体外共培养，以研究对MAPC：脾细胞直接接触的需求以及MAPC治疗对M1和M2巨噬细胞亚型凋亡和增殖的影响。结果分别在24和48小时时，通过MAPC治疗观察到脾细胞和血浆T调节细胞群显着增加。另外，MAPC疗法与皮质损伤后24、48和120小时时脑M2 / M1巨噬细胞比例的增加有关。活化的小胶质细胞与来自MAPC：脾细胞共培养的上清液的体外培养也显示M2 / M1比率增加。观察到的变化是继发于M1巨噬细胞凋亡的增加。结论数据显示，皮质损伤后的MAPC静脉内递送导致脾细胞和血浆中的T调节细胞增加，而局部M2 / M1巨噬细胞比例也相应增加。调节活化的小胶质细胞需要MAPC和脾细胞之间的直接接触，这为脾在MAPC介导的神经保护中的核心作用提供了进一步的证据。

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