LPS and TNFalpha induce SOCS3 mRNA and inhibit IL-6-induced activation of STAT3 in macrophages

Recent findings indicate that cytokine signaling can be modulated by other mediators of simultaneously activated signal transduction pathways. In this study we show that LPS and TNFalpha are potent inhibitors of IL-6-mediated STAT3 activation in human monocyte derived macrophages, rat liver macropha...

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Veröffentlicht in:	FEBS letters 1999-12, Vol.463 (3), p.365-370
Hauptverfasser:	Bode, J G, Nimmesgern, A, Schmitz, J, Schaper, F, Schmitt, M, Frisch, W, Häussinger, D, Heinrich, P C, Graeve, L
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Cell Line DNA-Binding Proteins - metabolism Gene Expression Regulation - drug effects Genes, Suppressor Humans Interleukin-6 - antagonists & inhibitors Kupffer Cells - drug effects Lipopolysaccharides - pharmacology Liver - cytology Liver - drug effects Liver - metabolism Macrophages - drug effects Macrophages - metabolism Male Mice Mitogen-Activated Protein Kinases - antagonists & inhibitors p38 Mitogen-Activated Protein Kinases Rats Rats, Wistar Signal Transduction - drug effects Signal Transduction - genetics STAT3 Transcription Factor Trans-Activators - metabolism Tumor Cells, Cultured Tumor Necrosis Factor-alpha - pharmacology
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Zusammenfassung:	Recent findings indicate that cytokine signaling can be modulated by other mediators of simultaneously activated signal transduction pathways. In this study we show that LPS and TNFalpha are potent inhibitors of IL-6-mediated STAT3 activation in human monocyte derived macrophages, rat liver macrophages and RAW 264.7 mouse macrophages but not in human hepatoma cells (HepG2) or in rat hepatocytes. Accordingly, LPS and TNFalpha were found to induce the expression of SOCS3 mRNA in each of the investigated type of macrophages but not in HepG2 cells. Using a specific inhibitor, evidence is presented that the p38 MAP kinase might be involved, especially for the inhibitory effect of TNFalpha.
ISSN:	0014-5793