BETA-ENDORPHIN BLUNTS PHOSPHATIDYLINOSITOL FORMATION DURING INVITRO ACTIVATION OF ISOLATED HUMAN-LYMPHOCYTES - PRELIMINARY-REPORT

We have previously described the regulatory effect of β-endorphin on three human cytotoxic cell populations. We confirmed the variable nature of these effects on human natural killer cell (NK) activity, showed mixed effects on the generation of cytotoxic T lymphocyte (CTL) activity, and demonstrated the reproducible suppression of lymphokine-activated killer cell (LAK) activity. We and others also observed mixed effects of β-endorphin on the proliferative response to mitogens and in mixed leukocyte reactions. In the study reported here, we test the effects of β-endorphin on the formation of phosphatidylinositol during cell activation. 32P-radiolabeled peripheral blood mononuclear cells obtained from normal adult donors and CD2-depleted subpopulations were activated with phytohemagglutinin or in a NK, LAK, or CTL protocol in the absence or presence of recombinant β-endorphin. The total lipidic extract was analyzed by thinlayer chromatography and autoradiography. The results of these studies indicate that β-endorphin blunts the formation of phosphatidylinositol by about 20% in the four systems studied and in all the donors tested. This effect is dose-dependent and is blocked in part by the opioid antagonist, naltrexone, suggesting involvement of the opioid receptor. © 1992.