Rescue effects of intravenous immunoglobulin on optic nerve degeneration in a rat model of neuromyelitis optica.

Abstract

Neuromyelitis optica (NMO) is an autoimmune inflammatory disease that predominantly attacks the optic nerve and spinal cord. This study evaluated the effect of administration of human IgG (hIgG) into the caudal vein on optic nerve degeneration in a rodent model of NMO. The optic nerves were exposed to AQP4-Ab-positive sera, and the administration of intravenous immunoglobulin (IVIG) was performed immediately, at 7days (cohort A) or at 7days and 10days (cohort B) after exposure to the sera. A reference group, similarly exposed to the serum, was treated with saline. Retinal ganglion cells (RGCs) labeled by the injection of Fluoro-Gold into the superior colliculus were counted in whole-mounted retina. RGCs labeled by the injection of Fluoro-Gold into the superior colliculus were counted in the whole-mounted retina. The number of RGCs 14days after optic nerve exposure to sera from patients with NMO was 1455±192/mm(2) (n=7) in cohort A, 1657±192/mm(2) (n=4) in cohort B, and 981±182/mm(2) (n=10) in the saline-treated reference group (p<0.001). Western blotting revealed that the content of neurofilament in the optic nerve of the hIgG-treated group in cohort A was significantly greater than that in the reference group (p=0.037). IVIG administration reduced optic nerve degeneration in a rat model of NMO-optic neuritis. IVIG could be used as a treatment in the acute phase of NMO.