| First Author | Carpenter GW | Year | 1994 |
| Journal | Brain Behav Immun | Volume | 8 |
| Issue | 3 | Pages | 185-203 |
| PubMed ID | 7865891 | Mgi Jnum | J:21187 |
| Mgi Id | MGI:69219 | Doi | 10.1006/brbi.1994.1018 |
| Citation | Carpenter GW, et al. (1994) Chronic morphine treatment suppresses CTL-mediated cytolysis, granulation, and cAMP responses to alloantigen. Brain Behav Immun 8(3):185-203 |
| abstractText | Exposure to opioid drugs (e.g., morphine) in vivo has been shown to suppress natural killer cell activity. However, the effects of in vivo exposure to opioids on cytotoxic T lymphocyte (CTL) activity has not been investigated. The administration of morphine (50.0 mg/kg, sc) to alloimmunized mice for 11 days resulted in a significant decrease in peritoneal and splenic CTL activity. Moreover, the intracellular content of serine esterases and esterase release by CD8+ effector cells from chronic morphine-treated mice was reduced compared to that of effector cells from vehicle-treated controls. In addition, the CD8+ cAMP response to alloantigen was diminished compared to CD(8+)-enriched cells from vehicle-treated animals. However, conjugate formation between effector and target and subsequent killing of target by effector cells did not reveal significant differences between vehicle- and chronic morphine-treated animals. Serum corticosterone and dehydroepiandrosterone levels were significantly lower in the chronic morphine-treated animals while proopiomelanocortin gene expression (exon 3) in splenic lymphocytes did not correlate with morphine-mediated suppression of CTL activity. These results indicate that CTL activity is sensitive to chronic morphine exposure, implicating opioids as important cofactors during viral infections in suppressing cell-mediated immunity. |
