Dobbs C M, Vasquez M, Glaser R, Sheridan J F
Department of Medical Microbiology and Immunology, College of Medicine, Ohio State University, Columbus 43210.
J Neuroimmunol. 1993 Nov-Dec;48(2):151-60. doi: 10.1016/0165-5728(93)90187-4.
A murine model of herpes simplex virus (HSV) infection was used to examine the roles of catecholamines and corticosterone in the restraint stress-induced suppression of viral immunity. Treatment of C57BL/6 mice with RU486, a glucocorticoid receptor antagonist, reversed the stress-induced diminution of cellularity in response to local HSV infection. Treatment of mice with both nadolol, a peripherally acting beta-adrenergic antagonist, and RU486 completely reversed the restraint stress-induced suppression of HSV-specific CTL activation. These findings demonstrate that both corticosterone and catecholamine-mediated mechanisms are operative in the stress-induced suppression of anti-viral cellular immunity.
