Enhancement of Murine Bone Marrow Macrophage Differentiation by β-Endorphin

Abstract

The present study was performed to investigate the effect of β-endorphin on macrophage colony-stimulating factor (M-CSF)-induced differentiation of macrophages from bone marrow cells in a semisolid culture system. β-endorphin increased the number of macrophage colonies when bone marrow cells were cultured in the presence of M-CSF plus lipopolysaccharide (LPS). This was not the case with LPS-unresponsive C3H/HeJ mouse bone marrow cells. α-endorphin and γ-endorphin were as effective as β-endorphin in enhancing the colony formation. Exogenous interleukin-1 (IL-1), but neither IL-6 nor tumor necrosis factor (TNF), collaborated with β-endorphin even in the absence of LPS, suggesting that IL-1 is a primary mediator of the effect of LPS. Indeed, anti-IL-1 antibody abolished the collaborative effect of β-endorphin with LPS. Moreover, IL-1 was effective even for C3H/HeJ mouse bone marrow cells. Naloxone, an antagonist of endorphins for opioid-receptors, completely abrogated the effect of β-endorphin. In a single-cell culture system, the collaboration between β-endorphin and IL-1 was revealed by the increase in number and size of macrophage colonies, but collaboration between β-endorphin and LPS did not occur. These results indicate that, in mixed cell culture, β-endorphin acts in concert with paracrinal IL-1 induced by LPS to enhance M-CSF-dependent macrophage differentiation from immature precursor cells. © 1995 by The American Society of Hematology.