Cocaine-mediated suppression of superoxide production by human peripheral blood mononuclear cells.

Cocaine, like opiates, modulates a variety of immune functions. In the present study, we investigated the effect of cocaine on superoxide anion (O2-) production, an index of a microbicidal activity, by cultured human peripheral blood mononuclear cells. Release of O2- was measured by superoxide dismutase-inhibitable reduction of ferricytochrome C in response to phorbol myristate acetate. Peripheral blood mononuclear cells cultured in the presence of cocaine (1 microM) for 48 hr released less (P less than .05) O2- than did nontreated control cells (95.1 +/- 10.2 vs. 57.9 +/- 6.6 nmol/10(7) cells/60 min, respectively). This suppressive effect was dose-dependent. Antibodies to transforming growth factor-beta, a cytokine inhibitory of monocyte O2- production, abrogated (P less than .01) cocaine-mediated suppression, suggesting that transforming growth factor-beta is involved in the suppression. Also, naloxone blocked (P less than .01) the suppressive effects of both cocaine and transforming growth factor-beta on O2- production, suggesting that the suppressive mechanism is naloxone-sensitive.