Mechanisms of stress-induced modulation of viral pathogenesis and immunity

J Neuroimmunol. Nov-Dec 1993;48(2):151-60. doi: 10.1016/0165-5728(93)90187-4.

Abstract

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Herpes Simplex / immunology
  • Immunity, Cellular / drug effects
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mifepristone / pharmacology
  • Nadolol / pharmacology
  • Stress, Physiological / immunology*
  • Virus Diseases / immunology*

Substances

  • Mifepristone
  • Nadolol