Department of Neurology, Faculty of Medicine and University Hospital Cologne, Germany; Center for Molecular Medicine Cologne (CMMC), University of Cologne, Germany.
Department of Neurology, Faculty of Medicine and University Hospital Cologne, Germany.
J Neuroimmunol. 2020 Jun 15;343:577218. doi: 10.1016/j.jneuroim.2020.577218. Epub 2020 Mar 20.
Data are sparse about mitochondrial damage in GBS and in its most frequently employed animal model, experimental autoimmune neuritis (EAN). We here characterized changes in mitochondrial content and morphology at different time points during EAN by use of ultrastructural imaging and immunofluorescent labelling. Histological examination revealed that demyelinated axons and their adjacent Schwann cells showed reduced mitochondrial content and remaining mitochondria appeared swollen with greater diameter in Schwann cells and unmyelinated axons. Our findings indicate that in EAN, particularly mitochondria in Schwann cells are damaged. Further studies are warranted to address whether these changes are amenable to novel, mitoprotective treatments.
关于吉兰-巴雷综合征(GBS)及其最常用的动物模型——实验性自身免疫性神经炎(EAN)中的线粒体损伤,相关数据较为匮乏。本研究通过超微结构成像和免疫荧光标记,在 EAN 不同时间点对线粒体含量和形态的变化进行了特征描述。组织学检查显示,脱髓鞘轴突及其相邻的施万细胞中的线粒体含量减少,剩余的线粒体在施万细胞和无髓鞘轴突中呈现肿胀,直径增大。我们的研究结果表明,在 EAN 中,特别是施万细胞中的线粒体受到了损伤。需要进一步研究这些变化是否可以通过新型的线粒体保护治疗来改善。