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Publication : Mu-opioid receptor mediates chronic restraint stress-induced lymphocyte apoptosis.

First Author  Wang J Year  2002
Journal  J Immunol Volume  169
Issue  7 Pages  3630-6
PubMed ID  12244154 Mgi Jnum  J:79236
Mgi Id  MGI:2387537 Doi  10.4049/jimmunol.169.7.3630
Citation  Wang J, et al. (2002) micro -Opioid Receptor Mediates Chronic Restraint Stress-Induced Lymphocyte Apoptosis. J Immunol 169(7):3630-6
abstractText  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, micro -opioid receptor knockout (MORKO) mice were used to investigate whether the micro -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-gamma 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 micro -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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