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Granulocyte colony-stimulating factor treatment protects rodents against lipopolysaccharide-induced toxicity via suppression of systemic tumor necrosis factor-alpha

Granulocyte colony-stimulating factor treatment protects rodents against lipopolysaccharide-induced toxicity via suppression of systemic tumor necrosis factor-alpha

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GÖRGEN, Ingrid, Thomas HARTUNG, Marcel LEIST, Marcus NIEHÖRSTER, Gisa TIEGS, Stefan UHLIG, Frank WEITZEL, Albrecht WENDEL, 1992. Granulocyte colony-stimulating factor treatment protects rodents against lipopolysaccharide-induced toxicity via suppression of systemic tumor necrosis factor-alpha. In: Journal of immunology. American Association of Immunologists. 149(3), pp. 918-924. ISSN 0022-1767. eISSN 1550-6606

@article{Gorgen1992-08-01Granu-51292, title={Granulocyte colony-stimulating factor treatment protects rodents against lipopolysaccharide-induced toxicity via suppression of systemic tumor necrosis factor-alpha}, url={https://www.jimmunol.org/content/149/3/918}, year={1992}, number={3}, volume={149}, issn={0022-1767}, journal={Journal of immunology}, pages={918--924}, author={Görgen, Ingrid and Hartung, Thomas and Leist, Marcel and Niehörster, Marcus and Tiegs, Gisa and Uhlig, Stefan and Weitzel, Frank and Wendel, Albrecht} }

<rdf:RDF xmlns:dcterms="http://purl.org/dc/terms/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:bibo="http://purl.org/ontology/bibo/" xmlns:dspace="http://digital-repositories.org/ontologies/dspace/0.1.0#" xmlns:foaf="http://xmlns.com/foaf/0.1/" xmlns:void="http://rdfs.org/ns/void#" xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > <rdf:Description rdf:about="https://kops.uni-konstanz.de/rdf/resource/123456789/51292"> <dc:contributor>Wendel, Albrecht</dc:contributor> <dc:contributor>Leist, Marcel</dc:contributor> <dc:creator>Leist, Marcel</dc:creator> <dc:rights>terms-of-use</dc:rights> <dc:language>eng</dc:language> <dc:contributor>Niehörster, Marcus</dc:contributor> <dc:contributor>Uhlig, Stefan</dc:contributor> <dc:creator>Tiegs, Gisa</dc:creator> <foaf:homepage rdf:resource="http://localhost:8080/jspui"/> <dc:creator>Weitzel, Frank</dc:creator> <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/> <dc:contributor>Hartung, Thomas</dc:contributor> <dc:contributor>Tiegs, Gisa</dc:contributor> <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2020-10-12T07:17:26Z</dc:date> <dc:creator>Uhlig, Stefan</dc:creator> <dc:contributor>Görgen, Ingrid</dc:contributor> <dc:contributor>Weitzel, Frank</dc:contributor> <dc:creator>Wendel, Albrecht</dc:creator> <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2020-10-12T07:17:26Z</dcterms:available> <dcterms:abstract xml:lang="eng">Pretreatment with recombinant human granulocyte CSF (G-CSF) protected mice in two different models of septic shock. Intravenous injection of 250 micrograms/kg G-CSF to mice prevented lethality induced by 5 mg/kg LPS. Injection of 50 micrograms/kg G-CSF protected galactosamine-sensitized mice against LPS-induced hepatitis. In either case, this protection was accompanied by a suppression of LPS-induced serum TNF activity. In contrast, when galactosamine-sensitized mice were pretreated with 50 micrograms/kg murine recombinant granulocyte/macrophage CSF instead of G-CSF and subsequently challenged with LPS, serum TNF activity was significantly enhanced and mortality was increased. The suppressive effect of G-CSF on LPS-induced TNF production was also demonstrated in rats. In vivo, no TNF was detectable in the blood of LPS-treated rats, which had been pretreated with G-CSF. Ex vivo, alveolar macrophages, bone marrow macrophages, Kupffer cells, or peritoneal macrophages prepared from G-CSF-treated rats produced significantly less TNF upon stimulation with LPS than corresponding populations from control rats. However, when these macrophage populations were incubated with G-CSF in vitro, LPS-induced TNF production was unaffected. These data suggest that the G-CSF-mediated suppression of TNF production is not a direct effect of G-CSF on macrophages. To examine whether, independent of the protection against LPS, G-CSF treatment still activated neutrophils, it was demonstrated that granulocytes from G-CSF-treated rats were primed for PMA-induced oxidative burst and for ionophore/arachidonic acid-stimulated lipoxygenase product formation. The experiments of this study support the notion that G-CSF is a negative feedback signal for macrophage-derived TNF-alpha production during Gram-negative sepsis.</dcterms:abstract> <dcterms:rights rdf:resource="https://rightsstatements.org/page/InC/1.0/"/> <dc:creator>Görgen, Ingrid</dc:creator> <dc:creator>Niehörster, Marcus</dc:creator> <bibo:uri rdf:resource="https://kops.uni-konstanz.de/handle/123456789/51292"/> <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/rdf/resource/123456789/28"/> <dcterms:title>Granulocyte colony-stimulating factor treatment protects rodents against lipopolysaccharide-induced toxicity via suppression of systemic tumor necrosis factor-alpha</dcterms:title> <dcterms:issued>1992-08-01</dcterms:issued> <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/rdf/resource/123456789/28"/> <dc:creator>Hartung, Thomas</dc:creator> </rdf:Description> </rdf:RDF>

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