ArticleThe Journal of clinical investigation1994
Potentiation by granulocyte macrophage colony-stimulating factor of lipopolysaccharide toxicity in mice.
Article in The Journal of clinical investigation, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04400929 (Using GM-CSF as a Host Directed Therapeutic Against COVID-19 - a Phase 2 Investigator Initiated Trial), which is not on this map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Using GM-CSF as a Host Directed Therapeutic Against COVID-19 - a Phase 2 Investigator Initiated Trial
Who cites it
14 citing papers in PubMed, 71 citations in OpenAlex.
- Chrysophanol-8-O-glucoside protects mice against acute liver injury by inhibiting autophagy in hepatic stellate cells and inflammatory response in liver-resident macrophages.Frontiers in pharmacology · 2022Article
- Alpha-hemolysin of uropathogenic Escherichia coli induces GM-CSF-mediated acute kidney injury.Mucosal immunology · 2020Article
- The antidepressant effects of GM-CSF are mediated by the reduction of TLR4/NF-ĸB-induced IDO expression.Journal of neuroinflammation · 2019Article
- Intravenous delivery of granulocyte-macrophage colony stimulating factor impairs survival in lipopolysaccharide-induced sepsis.PloS one · 2019Article
- SKLB023 protects mice against acute liver injury by inhibiting proinflammatory cytokine production in both T cells and macrophages.RSC advances · 2018Article
- The Neurokinin-1 Receptor Contributes to the Early Phase of Lipopolysaccharide-Induced FeverFrontiers in immunology · 2018Article
- Article
- Inhibitory effect of statins on inflammatory cytokine production from human bronchial epithelial cells.Clinical and experimental immunology · 2012Article
- GM-CSF signalling boosts dramatically IL-1 production.PloS one · 2011Article
- Granulocyte macrophage-colony stimulating factor (GM-CSF) augments acute lung injury via its neutrophil priming effects.Journal of Korean medical science · 2008Article
- Blockade of collagen-induced arthritis post-onset by antibody to granulocyte-macrophage colony-stimulating factor (GM-CSF): requirement for GM-CSF in the effector phase of disease.Arthritis research · 2001Article
- Article
- Theophylline accelerates human granulocyte apoptosis not via phosphodiesterase inhibition.The Journal of clinical investigation · 1997Article
- Differential alterations in plasma colony-stimulating factor concentrations in meningococcaemia.Clinical and experimental immunology · 1995Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.