Suppression of human B lymphocyte activation by beta-endorphin

The effects of beta-endorphin (beta-E) and contained peptides were investigated for their ability to regulate Staphylococcus aureus (SAC)-induced immunoglobulin secretion by human B lymphocytes. Co-culture of beta-E with SAC-stimulated peripheral blood-derived mononuclear cells, under serum-containing or serum-free conditions, resulted in a dose-dependent inhibition of immunoglobulin-secreting cell (ISC) formation. When the same cultures were assessed for class-specific Ig formation it was found that IgG-ISC were suppressed to a greater extent that IgA-ISC or IgM-ISC. In contrast to these results, beta-E was found to be unable to suppress SAC-induced lymphocyte proliferation. To map the suppressive activity associated with beta-E, truncated peptides based on the beta-E sequence were assessed for biological activity. The results indicated that peptides containing the N-terminal region of beta-E suppressed ISC formation. Moreover, methionine-enkephalin (beta-E 61-65) was found to be effective in suppressing ISC formation. beta-E-mediated suppression of IgG-specific ISC formation appears to involve classical receptor-ligand interaction as evidenced by the ability of naloxone to block suppression of ISC formation.