RT Journal Article
SR Electronic
T1 Systemic Morphine Administration Suppresses Genes Involved in Antigen Presentation
JF Molecular Pharmacology
JO Mol Pharmacol
FD American Society for Pharmacology and Experimental Therapeutics
SP 437
OP 442
DO 10.1124/mol.65.2.437
VO 65
IS 2
A1 Karen Beagles
A1 Anton Wellstein
A1 Barbara Bayer
YR 2004
UL http://molpharm.aspetjournals.org/content/65/2/437.abstract
AB Administration of opioids in both humans and animal models results in significant alterations in immune system responsiveness. Although the majority of studies have focused on phenotypic changes in immune cells after short- and long-term morphine administration, few studies have determined whether alterations in gene expression profiles accompany these effects. To address this question, rats were treated with either morphine (20 mg/kg) or saline, and changes in gene expression and function in blood leukocytes were examined. Within 2 h, morphine administration resulted in a decrease in blood leukocyte expression of the major histocompatibility complex class II (MHC II RT1.B β) (–3.27-fold) and related molecules, including the MHC II invariant chain (–2.73-fold). Furthermore, these changes in gene expression were accompanied by a significant decrease in surface MHC II RT1.B β protein expression, specifically on B lymphocytes. Morphine administration was also found to inhibit IL-4 induced up-regulation of MHC II RT1.B β cell surface expression on B lymphocytes. This is the first demonstration that receptors involved in antigen presentation are modified after systemic morphine administration. We propose that the inability of B lymphocytes to up-regulate key immune proteins, such as the MHC II molecule, after exposure to antigen-induced cytokine production may account for the increase in the susceptibility to bacterial and viral infections such as HIV in both drug abusers and patients receiving morphine.