Acute stress shortens the time to onset of experimental allergic encephalomyelitis in SJL/J mice.

Abstract Experimental allergic encephalomyelitis (EAE) is a murine model of multiple sclerosis (MS), an inflammatory condition of the central nervous system (CNS) resulting in focal demyelination due to the infiltration of sensitized T-leukocytes through the blood-brain barrier (BBB). While chronic stress models have been shown to reduce EAE, acute emotional stress appears to exacerbate many neuroin-flammatory disorders, including remitting-relapsing MS. This is the only study to our knowledge that examined the effect of acute stress on EAE. Immobilization of SJL/J mice for 60 min, at days 2 and 3 post-inoculation with proteolipid protein (PLP), resulted in symptoms of EAE becoming apparent 4 days earlier than in control mice. The possibility that this effect could be due to increased BBB permeability was investigated by detecting 99 Technetium ( 99 Tc) gluceptate extravasation into brain parenchyma post-stress utilizing a gamma camera. There was 80% increase in BBB permeability after 60 min of acute immobilization stress as compared to controls. These findings may help explain the earlier onset of EAE symptoms.