Microglia response in retina and optic nerve in chronic experimental autoimmune encephalomyelitis

被引:35
|
作者
Horstmann, Lioba [1 ]
Kuehn, Sandra [1 ]
Pedreiturria, Xiomara [2 ]
Haak, Kathrin [2 ]
Pfarrer, Christiane [3 ]
Dick, H. Burkhard [1 ]
Kleiter, Ingo [2 ]
Joachim, Stephanie C. [1 ]
机构
[1] Ruhr Univ Bochum, Univ Eye Hosp, Expt Eye Res Inst, Schornau 23-25, D-44892 Bochum, Germany
[2] Ruhr Univ Bochum, St Josef Hosp, Dept Neurol, Bochum, Germany
[3] Univ Vet Med Hannover, Dept Anat, Hannover, Germany
关键词
EAE; MOG; Multiple sclerosis; Microglia; Demyelination; Retinal ganglion cells; GANGLION-CELL LOSS; MULTIPLE-SCLEROSIS; MULLER CELLS; VISUAL FUNCTION; AXONAL INJURY; T-CELLS; IN-VIVO; NEURITIS; DEMYELINATION; INHIBITION;
D O I
10.1016/j.jneuroim.2016.06.008
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Experimental autoimmune encephalomyelitis (EAE) is a common rodent model for multiple sclerosis (MS). Yet, the long-term consequences for retina and optic nerve (ON) are unknown. C57BL/6 mice were immunized with an encephalitogenic peptide (MOG(35-55)) and the controls received the carriers or PBS. Clinical symptoms started at day 8, peaked at day 14, and were prevalent until day 60. They correlated with infiltration and demyelination of the ON. In MOG-immunized animals more microglia cells in the ONs and retinas were detected at day 60. Additionally, retinal ganglion cell (RGC) loss was combined with an increased macroglia response. At this late stage, an increased number of microglia was associated with axonal damage in the ON and in the retina with RGC loss. Whether glial activation contributes to repair mechanisms or adversely affects the number of RGCs is currently unclear. (C) 2016 Elsevier B.V. All rights reserved.
引用
收藏
页码:32 / 41
页数:10
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