Involvement of prostaglandins in LPS-mediated regulation of plasminogen activator synthesis by inflammatory macrophages.
We have previously shown that production of plasminogen activator by inflammatory macrophages can be inhibited by immunomodulators of bacterial origin, especially LPS. In these experiments, the contribution of prostaglandins to this control was investigated. We examined the effect of two prostaglandin synthetase blockers, indomethacin and diclofenac. These drugs do not modify per se the production of plasminogen activator but they can partially prevent the inhibitory effect of LPS. Since restoration was not complete when plasminogen activator production was strongly inhibited, it is suggested that the immunomodulator acts through a mechanism involving more than one pathway only one of which would be mediated by prostaglandins.
D000818:Animals; D001427:Bacterial Toxins / Q000494:pharmacology; D016861:Cyclooxygenase Inhibitors; D004008:Diclofenac / Q000494:pharmacology; D015232:Dinoprostone; D004731:Endotoxins; D004768:Enterotoxins / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D007249:Inflammation / Q000276:immunology*; D008070:Lipopolysaccharides / Q000502:physiology*; D008262:Macrophage Activation; D008264:Macrophages / Q000276:immunology* / Q000378:metabolism; D051379:Mice; D008815:Mice, Inbred Strains; D010960:Plasminogen Activators / Q000096:biosynthesis*; D011458:Prostaglandins E / Q000096:biosynthesis / Q000494:pharmacology / Q000502:physiology*
D001427:Bacterial Toxins; D016861:Cyclooxygenase Inhibitors; D004731:Endotoxins; D004768:Enterotoxins; D008070:Lipopolysaccharides; D011458:Prostaglandins E; C027952:salmonella toxin; D004008:Diclofenac; D010960:Plasminogen Activators; D015232:Dinoprostone; D007213:Indomethacin