Abstract
The effect of prostaglandtn E2, iloprost and cAMP on both nitric oxide and tumour necrosis factor-α release in J774 macrophages has been studied. Both prostaglandin E2 and iloprost inhibited, in a concentration-dependent fashion, the lipopolysaccharide-induced generation of nitric oxide and tumour necrosis factor-α. The inhibitory effect of these prostanoids seems to be mediated by an increase of the second messenger cAMP since it was mimicked by dibutyryl cAMP and potentiated by the selective type IV phosphodiesterase inhibitor RO-20-1724. Our results suggest that the inhibition of nitric oxide release by prostaglandin E2 and iloprost in lipopolysaccharide-activated J774 macrophages may be secondary to the inhibition of tumour necrosis factor-α generation, which in turn is likely to be mediated by cAMP.
Highlights
Macrophages activated with bacterial lipopolysaccharide release a variety of mediators including nitric oxide (NO), tumour necrosis factor (TNF-a) and prostaglandins, namely prostaglandin E2 (PGE2) and prostacyclin (PGI2).[1,2,3] The cytotoxic properties of activated macrophages depend, at least in part, on the biological activities of these mediators
We have shown that PGE2 and the stable analogue of PGI2, iloprost, inhibited the induction of NO synthase in lipopolysaccharide-activated J774 murine macrophages.[13]
We have shown that PGE2 and PG12, and its stable analogue iloprost, which are known to activate adenylate cyclase, inhibit the induction of macrophages
Summary
Macrophages activated with bacterial lipopolysaccharide release a variety of mediators including nitric oxide (NO), tumour necrosis factor (TNF-a) and prostaglandins, namely prostaglandin E2 (PGE2) and prostacyclin (PGI2).[1,2,3] The cytotoxic properties of activated macrophages depend, at least in part, on the biological activities of these mediators. Increasing evidence suggests that the interaction existing within the biological actions of NO, prostaglandins and TNF-ot may result in a mutual regulation of their synthesis and/or release. It has been reported that the release of TNF-0t by macrophages is inhibited by cAMP, a second messenger for both PGE2 and PGI2.1-2
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