Hyperacute allergic encephalomyelitis. A localized form produced by passive transfer and pertussis vaccine.

A hyperacute form of experimental allergic encephalomyelitis (EAE) has been produced previously by administering pertussis vaccine to rats actively immunized with neural antigen or given passive transfer of lymphoid cells from donors with EAE. Now, a localized form of hyperacute EAE has been produced within 1 day of passive transfer. The speed with which pertussis acts tends to exclude antibody production as the mechanism for conversion of EAE to the hyperacute form. With this rapid system, it has been found that pertussis, or its histamine-sensitizing factor, inhibited the host mononuclear cell component of the pervascular lesions. When the immune injury was sufficiently severe (high doses of donor EAE cells), the decrease in the number of mononuclear cells was accompanied by an increase in the amount of fibrin and the number of neutrophils in the lesions. This inverse relationship may be explained by the loss of the protective effect of mononuclear cells on vessels, a concept for which there is increasing evidence.