Nonspecific stress prevents relapses of experimental allergic encephalomyelitis in rats.
Rats with experimental allergic encephalomyelitis (EAE) develop paralysis, from which most of them recover. It has been hypothesized that spontaneous remission in EAE is due to the stress of paralysis and the subsequent hypersecretion of endogenous immunosuppressive adrenal glucocorticoids. Spontaneous relapse after a remission is thought to occur when the stress of paralysis and the adrenal response to it are terminated. In the present work, this theory has been tested in a newly developed relapsing form of EAE in rats. After an initial attack characterized by paralysis, the control rats had a remission and then a second episode of paralysis (relapse). In contrast, rats subjected to restraint during the remission period were protected from relapses. Injections of adrenal glucocorticoids during the remission had a similar protective effect. These findings support the hypothesis that remissions and relapses in EAE are caused by the occurrence and subsequent disappearance of the adrenals' immunosuppressive response to the stress of paralysis, because the addition of stress during the period of remission maintained the adrenals' hyperactive state and thereby prevented relapses.
D000311:Adrenal Glands / Q000276:immunology; D000818:Animals; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology*; D005260:Female; D005938:Glucocorticoids / Q000276:immunology; D007165:Immunosuppression Therapy; D009103:Multiple Sclerosis / Q000276:immunology; D051381:Rats; D011917:Rats, Inbred Lew; D012075:Remission, Spontaneous; D013312:Stress, Physiological / Q000276:immunology*
D005938:Glucocorticoids