Tumor necrosis factor stimulates interleukin-1 and prostaglandin E2 production in resting macrophages.
We have investigated the effect of tumor necrosis factor on the release of interleukin-1 and PGE2 from murine resident peritoneal macrophages. Tumor necrosis factor causes an increase in the production of interleukin-1 and PGE2 with a maximum induction for both noted at 5.9 X 10(-8) M. While indomethacin decreased tumor necrosis factor induced PGE2 production, this cyclooxygenase inhibitor augmented tumor necrosis factor induced interleukin-1 production. Our data suggests that tumor necrosis factor may be an important immunopotentiating agent in addition to its previously described cytolytic and metabolic activities.
D000818:Animals; D000917:Antibody Formation; D015232:Dinoprostone; D005260:Female; D006023:Glycoproteins / Q000494:pharmacology*; D006358:Hot Temperature; D007213:Indomethacin / Q000494:pharmacology; D007375:Interleukin-1 / Q000096:biosynthesis*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism; D051379:Mice; D008809:Mice, Inbred C3H; D008808:Mice, Inbred CBA; D011458:Prostaglandins E / Q000096:biosynthesis*; D014409:Tumor Necrosis Factor-alpha
D006023:Glycoproteins; D007375:Interleukin-1; D008070:Lipopolysaccharides; D011458:Prostaglandins E; D014409:Tumor Necrosis Factor-alpha; D015232:Dinoprostone; D007213:Indomethacin