Opposite effect of interferon-γ on PGE2 release from interleukin-1-stimulated human monocytes or fibroblasts

Stimulated monocytes produce prostaglandins (PGE 2 ) in response to lipopolysaccharide (LPS), Muramyl dipeptide (MDP) or Interleukin-1 (IL-1). This response could be modulated in different ways by Interferon-γ (IFN-γ). This lymphokine, known to potentiate IL-1 production by LPS- or MDP-stimulated monocytes, suppressed different Il-1 activities such as PGE 2 release by the same cells. By contrast, an impairement of suppression by IFN-γ was evidenced in rIL-1β-induced PGE 2 release from human dermal fibroblasts. Salmon calcitonin (sCT), another inhibitor of IL-1-induced bone resorption, was able to prime monocytes to potentiate PGE 2 elaboration by LPS, but failed to modulate PGE 2 liberation from either rIL-1β-stimulated monocytes or fibroblasts.