Microglia response in retina and optic nerve in chronic experimental autoimmune encephalomyelitis.
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.
Experimental Eye Research Institute, University Eye Hospital, Ruhr-University Bochum, In der Schornau 23-25, 44892 Bochum, Germany.
Lioba
L
Horstmann
Experimental Eye Research Institute, University Eye Hospital, Ruhr-University Bochum, In der Schornau 23-25, 44892 Bochum, Germany.
Sandra
S
Kuehn
Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Bochum, Germany.
Xiomara
X
Pedreiturria
Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Bochum, Germany.
Kathrin
K
Haak
Department of Anatomy, University of Veterinary Medicine Hannover, Germany.
Christiane
C
Pfarrer
Experimental Eye Research Institute, University Eye Hospital, Ruhr-University Bochum, In der Schornau 23-25, 44892 Bochum, Germany.
H Burkhard
HB
Dick
Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Bochum, Germany.
Ingo
I
Kleiter
Experimental Eye Research Institute, University Eye Hospital, Ruhr-University Bochum, In der Schornau 23-25, 44892 Bochum, Germany. Electronic address: stephanie.joachim@rub.de.
Stephanie C
SC
Joachim
D000704:Analysis of Variance; D000818:Animals; D001369:Axons / Q000187:drug effects / Q000473:pathology; D002135:Calcium-Binding Proteins / Q000378:metabolism; D000697:Central Nervous System Stimulants / Q000633:toxicity; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000139:chemically induced / Q000473:pathology*; D005620:Freund's Adjuvant / Q000633:toxicity; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008840:Microfilament Proteins / Q000378:metabolism; D017628:Microglia / Q000187:drug effects / Q000502:physiology*; D063308:Myelin-Oligodendrocyte Glycoprotein / Q000633:toxicity; D009900:Optic Nerve / Q000187:drug effects / Q000473:pathology*; D010446:Peptide Fragments / Q000633:toxicity; D010852:Picrotoxin / Q000633:toxicity; D051571:Protein Kinase C-alpha / Q000378:metabolism; D012160:Retina / Q000187:drug effects / Q000473:pathology*; D050819:Transcription Factor Brn-3A / Q000378:metabolism; D014746:Vimentin / Q000378:metabolism
D002135:Calcium-Binding Proteins; D000697:Central Nervous System Stimulants; D005620:Freund's Adjuvant; D005904:Glial Fibrillary Acidic Protein; D008840:Microfilament Proteins; D063308:Myelin-Oligodendrocyte Glycoprotein; D010446:Peptide Fragments; D010852:Picrotoxin; D051571:Protein Kinase C-alpha; D050819:Transcription Factor Brn-3A; D014746:Vimentin; C491049:Aif1 protein, mouse; C445081:myelin oligodendrocyte glycoprotein (35-55)
Demyelination; EAE; MOG; Microglia; Multiple sclerosis; Retinal ganglion cells