Article

Splenic norepinephrine depletion following acute stress suppresses in vivo antibody response.

Department of Integrative Physiology, University of Colorado, Campus Box 354, Boulder, Colorado 80309-0354, USA.
Journal of Neuroimmunology (impact factor: 2.96). 09/2005; 165(1-2):150-60. DOI:10.1016/j.jneuroim.2005.05.001 pp.150-60
Source: PubMed

ABSTRACT Exposure to an intense acute stressor immediately following immunization leads to a reduction in anti-KLH IgM, IgG, and IgG2a, but not IgG1. Stress also depletes splenic norepinephrine (NE) content. Immunization during pharmacological (alpha-methyl-p-tyrosine) or stress-induced splenic NE depletion results in antibody suppression similar to that found in rats immunized prior to stressor exposure. Prevention of splenic NE depletion during stress by tyrosine, but not pharmacological elevation (mirtazapine) of NE, resulted in normal antibody responses. These data support the hypothesis that splenic NE depletion is necessary and sufficient for stress-induced suppression of antibody to a T-cell dependent antigen.

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Keywords

alpha-methyl-p-tyrosine
 
anti-KLH IgM
 
antibody suppression
 
data support
 
intense acute stressor
 
normal antibody responses
 
pharmacological
 
pharmacological elevation
 
rats immunized
 
splenic NE depletion
 
splenic norepinephrine
 
stress-induced splenic NE depletion results
 
stress-induced suppression
 
stressor exposure
 
T-cell dependent antigen