Mechanisms whereby macrophage-derived nitric oxide is involved in morphine-induced immunomodulation.

Abstract

In vivo administration of morphine, whether acute or chronic, produces numerous alterations of immune status in both animals and humans. For instance, our laboratory and others demonstrated in rodent studies that morphine treatment produces a suppression of the mitogenic responsiveness of lymphocytes from the spleen and blood, a decrease in cytokine production by stimulated splenocytes, a depression of splenic natural killer cell activity, and a decrease in primary antibody responses.1,2,3 The means by which morphine produces immune alterations are unclear, but probably involve several systems within the organism, including the central nervous system, the autonomic nervous system and the neuroendocrine system, depending upon the immune compartment and immune measure being investigated and whether morphine is administered acutely or chronically.1,2,4