Brück W, Friede R L
Department of Neuropathology, University of Göttingen, F.R.G.
J Neuroimmunol. 1989 Nov;25(1):47-55. doi: 10.1016/0165-5728(89)90085-4.
Myelin phagocytosis in nerves undergoing Wallerian degeneration was shown to depend on their invasion by non-resident, hematogenous macrophages. This process can be studied in vitro using organ cultures of peripheral nerves exposed to cultured peritoneal macrophages. The present report concerns the effect of recombinant interferon-gamma (rIFN-gamma) on luminol-dependent chemiluminescence, macrophage migration and myelin phagocytosis in organ cultures. Chemiluminescence was activated by rIFN-gamma compared to untreated cells. The macrophage population was capable of activation at any phase of exposure to organ cultures. The engagement of macrophages in myelin phagocytosis, however, varied with the timing of the application of rIFN-gamma. Application from the start of the experiment led to activation of chemiluminescence and also to a complete inhibition of macrophage invasion of the organ culture, thus preventing myelin removal. Application of rIFN-gamma at a later phase of the experiment had no effect on cell invasion and also no detectable effect on the efficiency of myelin phagocytosis. There was no indication that myelin phagocytosis by itself activated chemiluminescence in untreated cultures. Phagocytosis of myelin appears to be a function of macrophages independent of activation causing production of oxygen radicals.
研究表明,在经历沃勒变性的神经中,髓鞘吞噬作用取决于非驻留性血源性巨噬细胞对其的侵袭。该过程可通过将外周神经器官培养物暴露于培养的腹膜巨噬细胞中,在体外进行研究。本报告关注重组干扰素-γ(rIFN-γ)对器官培养物中鲁米诺依赖性化学发光、巨噬细胞迁移和髓鞘吞噬作用的影响。与未处理的细胞相比,rIFN-γ激活了化学发光。巨噬细胞群体在暴露于器官培养物的任何阶段都能够被激活。然而,巨噬细胞参与髓鞘吞噬作用的情况随rIFN-γ应用时间的不同而有所变化。从实验开始就应用rIFN-γ会导致化学发光激活,同时还会完全抑制巨噬细胞对器官培养物的侵袭,从而阻止髓鞘的清除。在实验后期应用rIFN-γ对细胞侵袭没有影响,对髓鞘吞噬效率也没有可检测到的影响。没有迹象表明在未处理的培养物中,髓鞘吞噬作用本身会激活化学发光。髓鞘的吞噬作用似乎是巨噬细胞的一种功能,与导致氧自由基产生的激活作用无关。