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Research Article Free access | 10.1172/JCI117274

Potentiation by granulocyte macrophage colony-stimulating factor of lipopolysaccharide toxicity in mice.

G Tiegs, J Barsig, B Matiba, S Uhlig, and A Wendel

Department of Biochemical Pharmacology, Faculty of Biology, University of Konstanz, Germany.

Find articles by Tiegs, G. in: JCI | PubMed | Google Scholar

Department of Biochemical Pharmacology, Faculty of Biology, University of Konstanz, Germany.

Find articles by Barsig, J. in: JCI | PubMed | Google Scholar

Department of Biochemical Pharmacology, Faculty of Biology, University of Konstanz, Germany.

Find articles by Matiba, B. in: JCI | PubMed | Google Scholar

Department of Biochemical Pharmacology, Faculty of Biology, University of Konstanz, Germany.

Find articles by Uhlig, S. in: JCI | PubMed | Google Scholar

Department of Biochemical Pharmacology, Faculty of Biology, University of Konstanz, Germany.

Find articles by Wendel, A. in: JCI | PubMed | Google Scholar

Published June 1, 1994 - More info

Published in Volume 93, Issue 6 on June 1, 1994
J Clin Invest. 1994;93(6):2616–2622. https://doi.org/10.1172/JCI117274.
© 1994 The American Society for Clinical Investigation
Published June 1, 1994 - Version history
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Abstract

GM-CSF is known to prime leukocytes for inflammatory stimuli in vitro. The objective of this study was to investigate the role of GM-CSF in vivo in a systemic inflammatory reaction syndrome. The results demonstrate a potentiation of LPS toxicity by GM-CSF in a mortality model as well as in a septic liver failure model in mice. Pretreatment of animals with 50 micrograms/kg GM-CSF induced lethality within 24 h in mice challenged with a subtoxic dose of LPS while controls survived > 72 h. A monoclonal anti-GM-CSF antibody significantly protected against a lethal LPS dose. Serum GM-CSF was inducible by LPS and peaked at 2 h. GM-CSF pretreatment dramatically potentiated systemic TNF release and hepatotoxicity induced by a subtoxic dose of LPS in galactosamine-sensitized mice. Potentiation of LPS hepatotoxicity was possible until 30 min after LPS challenge. Polyclonal anti-GM-CSF IgG protected against septic liver failure in this model and attenuated serum TNF concentrations. In vitro an ex vivo experiments revealed that after GM-CSF pretreatment LPS-induced IL-1 release from bone marrow or spleen cells was also enhanced. These findings suggest that GM-CSF represents an endogenous enhancer of LPS-induced organ injury, possibly by potentiating the release of proinflammatory cytokines such as TNF and IL-1.

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