Opioid dependency and T-helper cell functions in rhesus monkey.
Administration of morphine sulfate to rhesus monkeys may activate the quiescent lymphocyte for proliferation, induce a transient increase in the T cell proliferative response to mitogens, and cause an enhanced interleukin-2 release from the mitogen-stimulated lymphocytes. However, longitudinal studies of the animals dependent upon morphine or L-a-acetyl-methadol, a long-acting opioid, revealed an overall immunosuppression of T helper functions. In vitro studies using morphine and its antagonist naloxone suggested that the immunosuppression was not a result of a direct interaction between the opioids and conventional opiate receptors which might have been present on the lymphocytes. The studies also showed the importance of measuring [3H]thymidine incorporation rather than its uptake into cells to assess T cell activation.
Chuang
L F
LF
Department of Medical Pharmacology and Toxicology, School of Medicine, University of California, Davis 95616.
Killam
K F
KF
Chuang
R Y
RY
D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology; D000818:Animals; D002455:Cell Division / Q000187:drug effects; D004195:Disease Models, Animal; D007273:Injections, Intramuscular; D007376:Interleukin-2 / Q000097:blood; D008213:Lymphocyte Activation; D008253:Macaca mulatta; D008297:Male; D008692:Methadyl Acetate / Q000494:pharmacology*; D008934:Mitogens; D009021:Morphine Dependence / Q000276:immunology*; D006377:T-Lymphocytes, Helper-Inducer / Q000187:drug effects*; D013936:Thymidine / Q000378:metabolism
D007376:Interleukin-2; D008934:Mitogens; D008692:Methadyl Acetate; D013936:Thymidine