The Effect of Morphine and Dago on the Proliferative Response of Murine Splenocytes
There is an increasing body of evidence supporting the existence of a neural-immune network in which endogenous opioids play a role as mediators (1–3). Endogenous opioids have been shown to have a number of immunomodulatory activities (4–7). The literature on the capacity of exogenous opioids to modify immune function is small, but provocative. Other laboratories have shown that in vivo administration of morphine by the intracerebral ventricular (icv) route to mice markedly depresses NK cell activity (8,9). Implanted morphine pellets suppress mitogenic responses in mice when cells are taken 72 hr post drug exposure (10). Peripheral blood mononuclear cells taken from addicts have suppressed capacity to form rosettes with sheep red blood cells (5) and morphine added to human T lymphocytes in vitro modulates rosette formation (4). The fact that intravenous drug abusers are among the high risk groups for contracting AIDS has led to the hypothesis that immunomodulation by the drugs themselves may be a cofactor in susceptibility to HIV-1.
KeywordsOpioid Receptor Endogenous Opioid Staphylococcal Enterotoxin Mitogen Response Receptor Selectivity
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