Differential regulation of tumor necrosis factor-alpha in human alveolar macrophages and peripheral blood monocytes: a cellular and molecular analysis.

American Journal of Respiratory Cell and Molecular Biology
R M StrieterS L Kunkel

Abstract

Human tumor necrosis factor-alpha (TNF), a mononuclear phagocyte (MO)-derived peptide, is increasingly being recognized for its pleomorphic immunologic effects. A number of studies have demonstrated that LPS can induce TNF synthesis, but data examining the production and regulation of TNF in human MO populations are lacking. In this study, we present data demonstrating that alveolar macrophages (AMO) and peripheral blood monocytes (PBM) obtained from 10 normal volunteers display a significant difference in both the production of TNF and their susceptibility to TNF regulation by prostaglandin E2 (PGE2) and dexamethasone (Dex). Adherent populations of PBM and AMO were incubated for 18 h in the presence of either LPS (10 micrograms/ml) alone, PGE2 for 1 h prior to LPS challenge, Dex for 1 h prior to LPS challenge, or control media alone. Cell-free supernatants were examined for TNF bioactivity and cellular TNF mRNA was assessed via in situ hybridization and Northern blot analysis. PGE2 and Dex treatment of PBM suppressed LPS-induced TNF production by 78% and 72%, respectively, while AMO-TNF production was suppressed by only 22% and 33%. The accumulation of TNF mRNA in PBM was reduced 63% by PGE2 and 45% by Dex, as assessed by lase...Continue Reading

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