Stimulated monocytes produce prostaglandins (PGE2) in response to lipopolysaccharide (LPS), Muramyl dipeptide (MDP) or Interleukin-1 (IL-1). This response could be modulated in different ways by Interferon-gamma (IFN-gamma). This lymphokine, known to potentiate IL-1 production by LPS- or MDP-stimulated monocytes, suppressed different Il-1 activities such as PGE2 release by the same cells. By contrast, an impairement of suppression by IFN-gamma was evidenced in rIL-1 beta-induced PGE2 release from human dermal fibroblasts. Salmon calcitonin (sCT), another inhibitor of IL-1-induced bone resorption, was able to prime monocytes to potentiate PGE2 elaboration by LPS, but failed to modulate PGE2 liberation from either rIL-1 beta-stimulated monocytes or fibroblasts.