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  • Title: Granulocyte colony-stimulating factor (G-CSF) reduces not only gram-negative but also gram-positive infection-associated proinflammatory cytokine release by interaction between Kupffer cells and leukocytes.
    Author: Busch CJ, Wanner GA, Menger MD, Vollmar B.
    Journal: Inflamm Res; 2004 May; 53(5):205-10. PubMed ID: 15105970.
    Abstract:
    OBJECTIVE AND DESIGN: An important principle for the beneficial effects of granulocyte colony-stimulating factor (G-CSF), a central mediator in the endogenous host response, is the reduction of systemic cytokine levels in various gram-negative models of sepsis and septic shock. There is debate, however, on whether G-CSF is protective also in gram-positive sepsis and acts directly or indirectly on macrophages and hepatic Kupffer cells (KC). METHODS: KC were harvested from either G-CSF-(200 microg/kg bw i.v.) or saline-pretreated Sprague-Dawley rats and stimulated in vitro for subsequent assessment of cytokine release over 24 h. RESULTS: Pretreatment with G-CSF led to a significant (p<0.05) inhibition of lipopolysaccharide (LPS)-induced release of TNF-alpha (-81%), IL-6 (-82%) and IL-1 beta (-57%). Exposure of KC to heat-killed Staphylococcus aureus (S. aureus/SAC) caused a 2- to 3-fold higher TNF-alpha release, but similar IL-6 levels when compared with those after LPS stimulation. Still, G-CSF proved to significantly reduce the release of both TNF-alpha and IL-6 upon KC exposure with SAC for 24h. Interestingly, in neutropenic animals (100mg/kg cyclophosphamide), G-CSF was not capable to blunt the LPS-induced cytokine release, indicating that the action of G-CSF on KC is not direct in nature but targets cellular communication and function of neutrophils. CONCLUSIONS: The present results demonstrate that pretreatment with G-CSF in vivo effectively prevents the overactivation of KC by both gram-negative and gram-positive bacterial substances, probably via modulation of neutrophil function. Thus, inhibition of proinflammatory cytokine response through G-CSF may represent a promising hepatoprotective approach during systemic inflammation.
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