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Stress‐Induced Neuroendocrine Modulation of Viral Pathogenesis and Immunity a
Author(s) -
SHERIDAN JOHN F.,
DOBBS CATHLEEN,
JUNG JAEHO,
CHU XIAOHONG,
KONSTANTINOS ALEXANDRIA,
PADGETT DAVID,
GLASER RONALD
Publication year - 1998
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1998.tb09618.x
Subject(s) - pathogenesis , immunity , modulation (music) , stress (linguistics) , immune system , immunology , virology , medicine , physics , philosophy , linguistics , acoustics
A bstract : Physical restraint (RST) was used to examine the interactions among the hypothalamic‐pituitary‐adrenal (HPA) axis, sympathetic nervous system, and the immune response to infection. In these studies, mice were infected with either herpes simplex virus (HSV) or influenza A/PR8 virus so that the impact of neuroendocrine activation could be assessed on disease pathophysiology and anti‐viral immunity. RST suppressed lymphadenopathy in draining lymph nodes, reduced mononuclear cellular infiltration in the lungs, and suppressed virus‐specific cytokine and cytolytic T‐cell responses. Blockade of type II glucocorticoid receptors (by RU486) restored cellularity and cytokine responses to both organs in restraint‐stressed, infected mice. Thus, the HPA axis modulated cell trafficking and T‐cell cytokine responses. However, RU486 treatment failed to restore cytolytic T‐cell responses. Blockade of β‐adrenergic receptors (by nadolol), in combination with RU486 treatment, fully restored cytolytic T‐cell responses, suggesting that catecholamines were involved in suppressing the virus‐specific CD8 + cytolytic T‐cell response. RST also modulated the local development or expression of antibody‐secreting cells (ASC) in the lungs draining lymph nodes, and spleen following infection of restrained mice. RST significantly suppressed the number of virus‐specific ASC (IgM, IgG and subclasses IgG1 and IgG2a) in the lungs, mediastinal (MLN) lymph nodes and spleen, while it enhanced the responses in the superficial cervical (SCV) lymph nodes. This observation of differential modulation of ASC responses in the MLN and SCV lymph nodes supports the concept of tissue‐specific immunoregulation in response to stress.