1. Opioids modulate interleukin-1 production and secretion by bone-marrow macrophages.
- Author
-
Apte RN, Durum SK, and Oppenheim JJ
- Subjects
- Animals, Bone Marrow Cells, Drug Synergism, Interleukin-1 metabolism, Lipopolysaccharides pharmacology, Macrophages metabolism, Mice, Naloxone pharmacology, Silicon Dioxide pharmacology, beta-Endorphin pharmacology, Endorphins pharmacology, Enkephalins pharmacology, Interleukin-1 biosynthesis, Macrophages drug effects, Protein Precursors pharmacology, beta-Endorphin analogs & derivatives
- Abstract
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.
- Published
- 1990
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