Opposite effect of Interferon-gamma on PGE2 release from Interleukin-1-stimulated human monocytes or fibroblasts.
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.
Friteau
L
L
Département de Biotechnologies, CNRS/Roussel, Romainville, France.
Francesconi
E
E
Lando
D
D
Dugas
B
B
Damais
C
C
D000119:Acetylmuramyl-Alanyl-Isoglutamine / Q000494:pharmacology; D002116:Calcitonin / Q000494:pharmacology; D002455:Cell Division; D015232:Dinoprostone / Q000378:metabolism*; D004357:Drug Synergism; D005347:Fibroblasts / Q000378:metabolism*; D006801:Humans; D007371:Interferon-gamma / Q000494:pharmacology*; D007375:Interleukin-1 / Q000378:metabolism / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D009000:Monocytes / Q000378:metabolism*; D011994:Recombinant Proteins / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D007375:Interleukin-1; D008070:Lipopolysaccharides; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D000119:Acetylmuramyl-Alanyl-Isoglutamine; C028815:salmon calcitonin; D007371:Interferon-gamma; D002116:Calcitonin; D015232:Dinoprostone