Transforming growth factor-beta 1 inhibits synthesis of cytokines in endotoxin-stimulated human whole blood.
Autor: | Karres I; Division of Trauma Surgery, University Hospital Zurich, Switzerland., Kremer JP, Steckholzer U, Kenney JS, Ertel W |
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Jazyk: | angličtina |
Zdroj: | Archives of surgery (Chicago, Ill. : 1960) [Arch Surg] 1996 Dec; Vol. 131 (12), pp. 1310-6; discussion 1316-7. |
DOI: | 10.1001/archsurg.1996.01430240064008 |
Abstrakt: | Objective: To determine the potency of transforming growth factor-beta (TGF-beta) for inhibiting proinflammatory cytokine synthesis in endotoxin-stimulated human whole blood. Design: Endotoxin-stimulated whole blood from healthy volunteers as an ex vivo model of endotoxemia was incubated with different concentrations of TGF-beta 1. Cytokine levels in plasma with a bioassay (for tumor necrosis factor alpha) or an enzyme-linked immunosorbent assay (for interleukin [IL]-1 beta and IL-6), messenger RNA (mRNA) expression with northern blotting, and protein levels with Western blotting were determined. Results: High TGF-beta 1 concentrations (> 100 pg/mL) inhibited (P < .05) secretion of tumor necrosis factor alpha, IL-1 beta, and IL-6 into lipopolysaccharide-stimulated whole blood, while low concentrations (< 50 pg/mL) were ineffective. Moreover, TGF-beta 1 inhibited mRNA expression of tumor necrosis factor alpha and IL-6 in a dose-dependent manner. In contrast, neither IL-1 beta mRNA expression nor IL-1 beta protein synthesis were attenuated by TGF-beta 1. Conclusion: Transforming growth factor-beta 1, with its downregulatory effect on the synthesis and release of proinflammatory cytokines by phagocytic cells, represents an inhibitor of endotoxin-induced inflammatory reactions. |
Databáze: | MEDLINE |
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