Opioids modulate interleukin-1 production and secretion by bone-marrow macrophages.
In the present study, we have assessed the effect of opioids (endorphins, enkephalins and neoendorphins) on production of IL-1 activity by bone-marrow-derived macrophages. None of the neuropeptides induced IL-1 production by itself. However, some of the opioids potentiated IL-1 production and release in macrophages concomitantly stimulated by lipopolysaccharide (LPS) or silica. LPS induced predominantly intracellular IL-1 activity, whereas most of the silica-induced IL-1 was released extracellularly. beta-Endorphin, leucine-enkephalin (leu-enkephalin) and beta-neoendorphin all potentiated both intracellular and extracellular release of IL 1 induced by either LPS or silica. In contrast, alpha-endorphin, methionine-enkephalin (metenkephalin) and alpha-neoendorphin did not influence IL-1 production or release. The potentiating effects of beta-endorphin on LPS-induced IL-1 production/secretion were inhibited by naloxone, pointing to an involvement of opioid receptors.
Apte
R N
RN
Biological Carcinogenesis Development Program Resources, Inc.
Durum
S K
SK
Oppenheim
J J
JJ
D000818:Animals; D001854:Bone Marrow Cells; D004357:Drug Synergism; D004723:Endorphins / Q000494:pharmacology*; D004745:Enkephalins / Q000494:pharmacology*; D007375:Interleukin-1 / Q000096:biosynthesis* / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism; D051379:Mice; D009270:Naloxone / Q000494:pharmacology; D011498:Protein Precursors / Q000494:pharmacology*; D012822:Silicon Dioxide / Q000494:pharmacology; D001615:beta-Endorphin / Q000031:analogs & derivatives* / Q000494:pharmacology
D004723:Endorphins; D004745:Enkephalins; D007375:Interleukin-1; D008070:Lipopolysaccharides; D011498:Protein Precursors; D009270:Naloxone; D001615:beta-Endorphin; C025681:alpha-neoendorphin; D012822:Silicon Dioxide; C030719:beta-neo-endorphin