Molecular Neurobiology Laboratory, Department of Neurology, Medical Faculty Heinrich Heine University, Moorenstrasse 5, 40225 Düsseldorf, Germany.
Cell Tissue Res. 2012 Jul;349(1):229-48. doi: 10.1007/s00441-012-1427-3. Epub 2012 May 22.
Recruitment of inflammatory cells is known to drive the secondary damage cascades that are common to injuries of the central nervous system (CNS). Cell activation and infiltration to the injury site is orchestrated by changes in the expression of chemokines, the chemoattractive cytokines. Reducing the numbers of recruited inflammatory cells by the blocking of the action of chemokines has turned out be a promising approach to diminish neuroinflammation and to improve tissue preservation and neovascularization. In addition, several chemokines have been shown to be essential for stem/progenitor cell attraction, their survival, differentiation and cytokine production. Thus, chemokines might indirectly participate in remyelination, neovascularization and neuroprotection, which are important prerequisites for CNS repair after trauma. Moreover, CXCL12 promotes neurite outgrowth in the presence of growth inhibitory CNS myelin and enhances axonal sprouting after spinal cord injury (SCI). Here, we review current knowledge about the exciting functions of chemokines in CNS trauma, including SCI, traumatic brain injury and stroke. We identify common principles of chemokine action and discuss the potentials and challenges of therapeutic interventions with chemokines.
众所周知，炎症细胞的募集会引发中枢神经系统（CNS）损伤中常见的继发性损伤级联反应。趋化因子是趋化性细胞因子，其表达的变化协调着细胞的激活和浸润到损伤部位。通过阻断趋化因子的作用来减少募集的炎症细胞数量已被证明是一种很有前途的方法，可以减少神经炎症，改善组织保存和新生血管形成。此外，已经证明几种趋化因子对于干细胞/祖细胞的吸引、存活、分化和细胞因子产生是必不可少的。因此，趋化因子可能间接地参与髓鞘再生、新生血管形成和神经保护，这是创伤后中枢神经系统修复的重要前提。此外，CXCL12 在存在生长抑制性中枢神经系统髓鞘的情况下促进神经突生长，并增强脊髓损伤（SCI）后的轴突发芽。在这里，我们回顾了趋化因子在中枢神经系统创伤（包括 SCI、创伤性脑损伤和中风）中的令人兴奋的功能的现有知识。我们确定了趋化因子作用的共同原则，并讨论了趋化因子治疗干预的潜力和挑战。
