Mirski Roni, Reichert Fanny, Klar Avihu, Rotshenker Shlomo
Department of Anatomy and Cell Biology, Hebrew University-Hadassah Medical School, P.O.B. 12272, Jerusalem 91120, Israel.
J Neuroimmunol. 2003 Jul;140(1-2):88-96. doi: 10.1016/s0165-5728(03)00179-6.
The hematopoietic factor and inflammatory cytokine GM-CSF is involved in PNS and CNS injury and disease, and in macrophage and microglia function regulation. We presently document that injury to PNS axons induces in vivo production of GM-CSF-inhibitor and GM-CSF-augmenter activities. GM-CSF-inhibitor activity was detected in extract and conditioned medium (CM) of injured PNS but not in extract of intact PNS, and was removed from CM by GM-CSF affinity chromatography, suggesting it is carried by a secreted GM-CSF binding molecule. CM further displayed GM-CSF-augmenter activity along with GM-CSF-inhibitor activity but at contrasting concentrations; augmentation at lowest and inhibition at highest. GM-CSF activity is thus regulated during Wallerian degeneration (WD); augmenter activity characterizes the onset and inhibitor activity the later stages of WD.
造血因子和炎性细胞因子粒细胞-巨噬细胞集落刺激因子（GM-CSF）参与外周神经系统（PNS）和中枢神经系统（CNS）的损伤与疾病，以及巨噬细胞和小胶质细胞功能的调节。我们目前证明，PNS轴突损伤可在体内诱导GM-CSF抑制剂和GM-CSF增强剂活性的产生。在损伤的PNS提取物和条件培养基（CM）中检测到GM-CSF抑制剂活性，但在完整PNS的提取物中未检测到，并且通过GM-CSF亲和层析从CM中去除了该活性，这表明它由一种分泌的GM-CSF结合分子携带。CM还显示出GM-CSF增强剂活性以及GM-CSF抑制剂活性，但浓度相反；在最低浓度时增强，在最高浓度时抑制。因此，在华勒氏变性（WD）过程中GM-CSF活性受到调节；增强剂活性表征WD的起始阶段，而抑制剂活性表征WD的后期阶段。
