Abstract

Experimental allergic encephalomyelitis (EAE) has been a well established animal model of postvaccinatal demyelinating diseases occurring in humans. Therefore elucidation of its pathogenesis would be very critical for the understanding of various human demyelinating diseases including multiple sclerosis. This study was performed to characterize the infiltrating cells in inflammatory sites and analyze the nature of the damage of blood brain barrier in experimental allergic encephalomyelitis. Experimental allergic encephalomyelitis was produced by administering homologous spinal cord homogenate together with complete Freund's adjuvant in guinea pigs. Immunostainings on guinea pig IgG, IgM, IgA and muramidase were performed by peroxidase-antiperoxidase or indirect immunofluorescent methods. The blood-brain barrier change was assessed by administering fluorescent Evans blue. Following results were made. In juvenile animals, both clinical findings and histopathologic changes were first noted by 3 weeks after injection and progressed during the whole experimental period. However, these findings were delayed in onset and low in incidence in adult animals. The clinical and pathologic changes started from the caudal portions and extended rostrally. The blood-brain barrier (BBB) was damaged and progressed starting also from the caudal portion of the spinal cord. The BBB changes were more severe in young animal than adult animals. Those changes preceded th histologic alterations. It is suggested that the BBB susceptibility is responsible for the caudal onset of histologic changes. Although the lesion has been thought to be induced by T-cell mediated hypersensitivity, infiltrating cells consisted mainly of muramidase positive histiocytes. A few immunoglobulin positive B cells or plasma cells could also be demonstrated in the lesion. The former usually infiltrated the parenchyme and the latter remained around the small or medium-sized vessels.