Mechanisms of stress-induced modulation of viral pathogenesis and immunity.
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.
Dobbs
C M
CM
Department of Medical Microbiology and Immunology, College of Medicine, Ohio State University, Columbus 43210.
Vasquez
M
M
Glaser
R
R
Sheridan
J F
JF
D000818:Animals; D006561:Herpes Simplex / Q000276:immunology; D007111:Immunity, Cellular / Q000187:drug effects; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D015735:Mifepristone / Q000494:pharmacology; D009248:Nadolol / Q000494:pharmacology; D013312:Stress, Physiological / Q000276:immunology*; D014777:Virus Diseases / Q000276:immunology*
D015735:Mifepristone; D009248:Nadolol