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

•Brain and optic nerve inflammation remained persistent in chronic EAE.•A secondary retinal macroglia response occurred 60 days after EAE induction.•Resting microglia cells increased in retina and optic nerve at late stages of EAE.•Only ganglion cells are affected in retina at day 60.

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 (MOG35–55) 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.

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