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Opioid receptors of subtypes delta, kappa, and mu similar to those found in brain cells have been identified in immune cells. The current study demonstrates by competitive polymerase chain reaction the treatment of human lymphocytic cells with morphine resulting in an increased amount of gene expression of mu opioid receptors. Antibodies against the MOR-1, the neuronal mu opioid receptor, were used in Western blot analysis of mu proteins and the results revealed a single band of approximately 50 kDa, the intensity of which was increased by morphine treatment. Similar results of mu opioid receptor activation were observed when monkey lymphocytes were treated with morphine. These studies suggest that in addition to causing an immune effect through communication with the neuroendocrine system, the psychoactive drug morphine may modulate immune functions by acting directly on the mu opioid receptors expressed on lymphocytes., (Copyright 2000 Academic Press.)

We have previously demonstrated that administering morphine sulfate to rhesus monkeys alters the cell-mediated as well as humoral immune responses of these primates. Furthermore, morphine treatment greatly reduces the chemotactic and phagocytotic activities of primate polymorphonuclear (PMN) cells. The present study describes the identification and isolation of mRNA encoding the mu opioid receptor gene sequence from human and monkey immune cells. Through the use of primer sequences designed from the human brain mu opioid receptor cDNA sequence, specific opioid receptor segments in mRNA transcripts were amplified, cloned, and sequenced. The mu opioid receptor gene was therefore found expressed in the following cell types: CEM x174 (a hybrid of human T and B cells), Raji (human B cells), human CD4+ cells, human monocytes/macrophages, human PMN, monkey peripheral blood mononuclear cells (PBMC), and monkey PMN. These studies present the first evidence to demonstrate that cells of human and monkey immune systems constitutively express mu opioid receptor mRNA.