Chemokines in CNS injury and repair.
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.
Molecular Neurobiology Laboratory, Department of Neurology, Medical Faculty Heinrich Heine University, Moorenstrasse 5, 40225 Düsseldorf, Germany.
Anne
A
Jaerve
Hans Werner
HW
Müller
D002490:Central Nervous System / Q000276:immunology* / Q000293:injuries* / Q000473:pathology; D018925:Chemokines / Q000378:metabolism*; D006801:Humans; D019707:Receptors, Chemokine / Q000378:metabolism; D015398:Signal Transduction / Q000276:immunology; D014945:Wound Healing
D018925:Chemokines; D019707:Receptors, Chemokine