Experimental allergic encephalomyelitis(EAE) has been a well established animal model
of postvaccinatal demyelinating disease 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 the 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.
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