BETA-ENDORPHIN ENHANCES PHAGOCYTOSIS OF LATEX-PARTICLES IN MOUSE PERITONEAL-MACROPHAGES

The effects of beta-endorphin (beta End) on phagocytosis in peritoneal macrophages were examined by using flow cytometry (FCM). beta End enh anced phagocytosis in a dose-dependent manner. Leucine-enkephalin (Leu -Enk), methionine-enkephalin (Met-Enk), alpha-endorphin (alpha End), g amma-endorphin (gamma End), alpha End (18-31) and beta End (28-31) had no such activity. beta End (1-27) and beta End (6-31) enhanced phagoc ytosis less effectively than beta End did. Naloxone did not inhibit th e enhancement of phagocytosis induced by beta End. Unstimulated contro l phagocytosis was partially suppressed in Ca2+-free EGTA-containing s olution and even in this solution beta End enhanced phagocytosis. Howe ver, the enhancement was suppressed in the solution containing BAPTA-A M. The present study showed that beta End enhanced extracellular Ca2([Ca2+](o))-dependent and -independent phagocytosis and that the enhan cement is largely dependent on intracellular Ca2+ ([Ca2+](i)). These r esults support the contention that beta End is one of the mediators th at modulates the immune system.