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beta-Endorphin enhances phagocytosis of latex particles in mouse peritoneal macrophages
1Department of Physiology, Shimane Medical University, Izumo, Japan.
Abstract:
The effects of beta-endorphin (beta End) on phagocytosis in peritoneal macrophages were examined by using flow cytometry (FCM). Beta End enhanced phagocytosis in a dose-dependent manner. Leucine-enkephalin (Leu-Enk), methionine-enkephalin (Met-Enk), alpha-endorphin (alpha End), gamma-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 phagocytosis less effectively than beta End did. Naloxone did not inhibit the enhancement of phagocytosis induced by beta End. Unstimulated control phagocytosis was partially suppressed in Ca2(+)-free EGTA-containing solution and even in this solution beta End enhanced phagocytosis. However, the enhancement was suppressed in the solution containing BAPTA-AM. The present study showed that beta End 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 beta End is one of the mediators that modulates the immune system.
Insights
Beta-endorphin (beta End) enhances macrophage phagocytosis in a dose-dependent way. This effect relies on intracellular calcium, suggesting beta-endorphin modulates the immune system.
Area of Science:
- Immunology
- Neuroendocrinology
Background:
- Phagocytosis is a key immune process.
- Beta-endorphin (beta End) is a peptide hormone with known immunomodulatory roles.
Purpose of the Study:
- To investigate the effect of beta-endorphin on phagocytosis in peritoneal macrophages.
- To determine the role of calcium ions in beta-endorphin-mediated phagocytosis.
Main Methods:
- Flow cytometry (FCM) was used to quantify phagocytosis.
- Experiments were conducted in varying calcium concentrations and with calcium chelators (EGTA, BAPTA-AM).
Main Results:
- Beta-endorphin dose-dependently enhanced macrophage phagocytosis.
- Other endorphins and enkephalins showed no such activity.
- The enhancement was dependent on both extracellular and intracellular calcium, primarily intracellular calcium ([Ca2+]i).
Conclusions:
- Beta-endorphin enhances phagocytosis through a mechanism involving intracellular calcium signaling.
- Beta-endorphin acts as a modulator of the immune system, influencing macrophage function.