β-Endorphin Enhances Phagocytosis of Latex Particles in Mouse Peritoneal Macrophages

The effects of β-endorphin (βEnd) on phagocytosis in peritoneal macrophages were examined by using flow cytometry (FCM). βEnd enhanced phagocytosis in a dose-dependent manner. Leucine—enkephalin (Leu-Enk), methionine—enkephalin (Met—Enk), α-endorphin (αEnd), γ-endorphin (γEnd), αEnd (18–31) and βEnd (28–31) had no such activity. βEnd (1–27) and βEnd (6–31) enhanced phagocytosis less effectively than βEnd did. Naloxone did not inhibit the enhancement of phagocytosis induced by βEnd. Unstimulated control phagocytosis was partially suppressed in Ca²⁺-free EGTA-containing solution and even in this solution βEnd enhanced phagocytosis. However, the enhancement was suppressed in the solution containing BAPTA-AM. The present study showed that βEnd enhanced extracellular Ca²⁺ ([Ca²⁺]_o)-dependent and -independent phagocytosis and that the enhancement is largely dependent on intracellular Ca²⁺ ([Ca²⁺]_i). These results support the contention that βEnd is one of the mediators that modulates the immune system.