system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Cells, Cultured, Gram-Negative Bacterial Infections, Gram-Positive Bacterial Infections, Granulocyte Colony-Stimulating Factor, Interleukin-1, Interleukin-6, Kupffer Cells, Leukocytes, Lipopolysaccharides, Male, Neutropenia, Protective Agents, Rats, Rats, Sprague-Dawley, Time Factors, Tumor Necrosis Factor-alpha.
user
Reduces granulocyte colony-stimulating factor ( G-CSF ) only gram-negative but also gram-positive infection-associated proinflammatory cytokine release by interaction between Kupffer cells and leukocytes? Context: 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). 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. 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.
assistant
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. Final Decision: no