Lipopolysaccharide/endotoxin induces IL-18 via CD14 in human peripheral blood mononuclear cells in vitro

IL-18 shares activities with IL-12 in generating T-helper 1 cells and cytokine response. It mediates LPS/endotoxin lethality by IL-12 independent interferon-γ synthesis and it induces bacteria-related organ failure. As peripheral blood mononuclear cells (PBMC) are potent producers of IL-18, we studi...

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Hauptverfasser: Manigold, Tobias (VerfasserIn) , Böcker, Ulrich (VerfasserIn) , Traber, Petra Sieglinde (VerfasserIn) , Si, Tuan-Dong (VerfasserIn) , Kurimoto, Masashi (VerfasserIn) , Hanck, Christoph (VerfasserIn) , Singer, Manfred V. (VerfasserIn) , Rossol, Siegbert (VerfasserIn)
Dokumenttyp: Article (Journal) Editorial
Sprache:Englisch
Veröffentlicht: 2000
In: Cytokine
Year: 2000, Jahrgang: 12, Heft: 12, Pages: 1788-1792
ISSN:1096-0023
DOI:10.1006/cyto.2000.0783
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1006/cyto.2000.0783
Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S104346660090783X
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Verfasserangaben:Tobias Manigold, Ulrich Böcker, Petra Traber, Tuan Dong-Si, Masashi Kurimoto, Christoph Hanck, Manfred V. Singer, Siegbert Rossol

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520 |a IL-18 shares activities with IL-12 in generating T-helper 1 cells and cytokine response. It mediates LPS/endotoxin lethality by IL-12 independent interferon-γ synthesis and it induces bacteria-related organ failure. As peripheral blood mononuclear cells (PBMC) are potent producers of IL-18, we studied the regulation of IL-18 upon exposure to LPS and Staphylococcus aureus (SAC) in vitro. Freshly isolated PBMC constitutively expressed IL-18 mRNA. After unstimulated preincubation for 48h, however, IL-18 transcripts were nearly not detectable by RT-PCR, but inducible by LPS or SAC (P<0.01). Both LPS and SAC were potent stimuli of IL-18 protein secretion (P<0.01). LPS-mediated IL-18 gene expression and secretion was CD14-dependent and significantly inhibited by co-incubation of PBMC with neutralizing CD14 antibody (P<0.01). We conclude that LPS-driven IL-18 is dependent on the expression of costimulatory factors and that IL-18 inhibition might attenuate IL-18-related toxic effects. 
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