The effects and mechanism of bone marrow stromal cells for spinalcord injury

移植MSC减轻SCI后炎症的确切机制尚不清楚。移植的MSC在损伤的脊髓内迁移，而不分化成胶质细胞或神经元成分。MSC移植与SCI环境的显著变化相关，IL-4和IL-13水平显著升高，TNF-α和IL-6水平降低。这与交替活化的巨噬细胞（M2表型：iNOS-1或CD 206阳性）数量增加和经典活化的巨噬细胞（M1表型：iNOS或CD 16/32阳性）数量减少同时相关。这些变化与MSC移植组的功能性运动恢复有关，这与保留的轴突、较少的瘢痕组织形成和增加的髓鞘陪练有关。我们的研究结果表明，急性移植MSC SCI后改变炎症环境的巨噬细胞表型从M1到M2，这可能会减少在亚急性/慢性期损伤后的抑制性瘢痕组织的影响，为轴突延伸和功能恢复提供一个宽松的环境。

The precise mechanisms through which transplanted MSC attenuate inflammation after SCI are still unclear. The transplanted MSC migrated within the injured spinal cord without differentiating into glial or neuronal elements. MSC transplantation was associated with marked changes in the SCI environment, with significant increases in IL-4 and IL-13 levels reductions in TNF-α and IL-6 levels. This was associated simultaneously with increased numbers of alternatively activated macrophages (M2 phenotype: arginase -1 or CD206-positive) and decreased numbers of classically activated macrophages (M1 phenotype: iNOS or CD16/32-positive). These changes were associated with functional locomotion recovery in the MSC transplanted group, which correlated with preserved axons, less scar tissue formation and increased myelin sparring. Our results suggested that acute transplantation of MSC after SCI modified the inflammatory environment by shifting the macrophage phenotype from M1 to M2, and that this may reduce the effects of the inhibitory scar tissue in the subacute/chronic phase after injury to provide a permissive environment for axonal extension and functional recovery.