Beta-endorphin regulates interleukin 1 production and release by murine bone marrow macrophages

The role of the neuropeptide beta-endorphin on interleukin 1 (IL-1) production by murine bone marrow-derived macrophages was assessed. Beta-endorphin by itself did not induce IL-1 generation. However, over a wide range of concentrations (10(-6)-10(-14) M) beta-endorphin potentiated lipopolysaccharide (LPS)- or silica-induced production of intracellular and extracellular IL-1. This enhancement by beta-endorphin was most evident when using suboptimal doses of LPS. Naloxone, a competitive inhibitor of beta-endorphin opioid receptor interactions, abrogated the enhancing effects of beta-endorphin on LPS-induced IL-1 production. Furthermore, LPS-induced IL-1 production by macrophages (in the absence of added beta-endorphin) was also partially inhibited following treatment with naloxone, suggesting that opioids derived from activated macrophages may also modulate IL-1 generation and secretion. Thus, beta-endorphin-opioid receptor interactions result in enhanced production of immunomodulators such as IL-1.