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* Department of Pharmacology, University of Minnesota, Minneapolis, MN 55455;
Department of Surgery, Veterans Affairs Medical Center, Minneapolis, MN 55417; and
North Memorial Medical Center, Robbinsdale, MN 55422
Psychological stress is associated with immunosuppression in both
humans and animals. Although it was well established that psychological
stressors stimulate the hypothalamic-pituitary-adrenal axis and the
sympathetic nervous system, resulting in the release of various
hormones and neurotransmitters, the mechanisms underlying these
phenomena are poorly understood. In this study, µ-opioid receptor
knockout (MORKO) mice were used to investigate whether the µ-opioid
receptor mediates the immunosuppression induced by restraint stress.
Our results showed that wild-type (WT) mice subjected to chronic 12-h
daily restraint stress for 2 days exhibited a significant decrease in
splenocyte number with a substantial increase in apoptosis and CD95
(Fas/APO-1) expression of splenocytes. The effects are essentially
abolished in MORKO mice. Furthermore, inhibition of splenic lymphocyte
proliferation, IL-2, and IFN-
production induced by restraint stress
in WT mice was also significantly abolished in MORKO mice.
Interestingly, both stressed WT and MORKO mice showed a significant
elevation in plasma corticosterone and pituitary proopiomelanocortin
mRNA expression, although the increase was significantly lower in MORKO
mice. Adrenalectomy did not reverse restraint stress-induced
immunosuppression in WT mice. These data clearly established that the
µ-opioid receptor is involved in restraint stress-induced immune
alterations via a mechanism of apoptotic cell death, and that the
effect is not mediated exclusively through the glucocorticoid
pathway.
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