Trace levels of bacterial lipopolysaccharide prevent interferon-gamma or tumor necrosis factor-alpha from enhancing mouse peritoneal macrophage respiratory burst capacity.

摘要: Preexposure of resident mouse peritoneal macrophages for 1 hr to traces bacterial lipopolysaccharide (LPS) (less than or equal ng/ml) rendered the cells refractory activation by recombinant interferon-gamma (rIFN gamma) tumor necrosis factor-alpha (rTNF alpha), as evaluated release H2O2 upon stimulation with phorbol myristate acetate. Inhibition persisted at least 4 days. Fifty percent inhibition mediated rIFN gamma followed exposure 10 pg/ml LPS. rTNF alpha was achieved Such low levels LPS exposures (concentration X time) are far below those reported many other actions on host cells. partially prevented cyclooxygenase inhibitors indomethacin, ibuprofen, and acetylsalicylic acid. Exogenous prostaglandins PGE1 PGE2, 3',5'-cyclic adenosine monophosphate analog dibutyryl cyclic (cAMP), mimicked inhibitory effect in a dose-dependent manner, consistent hypothesis that formation endogenous products response may elevate intracellular cAMP latter mediate observed inhibition. In addition, neutralizing antibody against IFN beta selectively gamma, but not alpha. This suggests and/or induced also contributed gamma. Thus, afford microorganisms means which interfere immunologically enhancement respiratory burst-dependent antimicrobial capacity macrophages.