Granulocyte colony-stimulating factor enhances pulmonary host defenses in normal and ethanol-treated rats.

@article{Nelson1991GranulocyteCF,
  title={Granulocyte colony-stimulating factor enhances pulmonary host defenses in normal and ethanol-treated rats.},
  author={Steve Nelson and W. Summer and Gregory J. Bagby and C Nakamura and L Stewart and G Lipscomb and Jeffrey W. Andresen},
  journal={The Journal of infectious diseases},
  year={1991},
  volume={164 5},
  pages={
          901-6
        }
}
Ethanol suppresses functions of the polymorphonuclear leukocyte (PMNL), seriously compromising normal host defenses against pneumonia. Because granulocyte colony-stimulating factor (G-CSF) augments the number and function of PMNL, the effect of G-CSF on the antibacterial defenses of the lung in normal and acutely intoxicated rats was studied. Animals received G-CSF or vehicle twice a day for 2 days, then ethanol or saline, followed by challenge with Klebsiella pneumoniae. K. pneumoniae elicited… 
Granulocyte colony-stimulating factor prevents ethanol-induced impairment in host defense in septic rats.
TLDR
It is demonstrated that G-CSF is a potent immunomodulator that stimulates neutrophil recruitment selectively to the site of infection and that can be used to ameliorate the ethanol-induced impairment in bacterial host defense.
Granulocyte colony-stimulating factor modulates the pulmonary host response to endotoxin in the absence and presence of acute ethanol intoxication.
TLDR
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Granulocyte colony-stimulating factor protects control rats but not ethanol-fed rats from fatal pneumococcal pneumonia.
TLDR
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Suppression of the granulocyte colony-stimulating factor response to Escherichia coli challenge by alcohol intoxication.
TLDR
The results support the postulate that alcohol-induced inhibition of TNF alpha directly contributes to the adverse effects of alcohol on PMN function by suppressing the normal autocrine amplification pathway responsible for G-CSF production.
Pretreatment with Granulocyte Colony-Stimulating Factor Attenuates the Inflammatory Response but Not the Bacterial Load in Cerebrospinal Fluid during Experimental Pneumococcal Meningitis in Rabbits
TLDR
G-CSF pretreatment attenuates meningeal inflammation and enhances systemic bacterial killing in an experimental pneumococcal meningitis model in rabbits.
The Effects of Granulocyte Colony-Stimulating Factor and Neutrophil Recruitment on the Pulmonary Chemokine Response to Intratracheal Endotoxin
TLDR
G-CSF augments PMN recruitment and, thereby, lowers local chemokine levels, which may be one mechanism resulting in the subsidence of the host proinflammatory response.
Granulocyte colony-stimulating factor worsens the outcome of experimental Klebsiella pneumoniae pneumonia through direct interaction with the bacteria.
TLDR
The paradoxical finding that mortality from infection was significantly increased when animals received G-CSF before induction of pneumonia is shown, indicating an impairment rather than an enhancement of antibacterial mechanisms.
Acute ethanol intoxication suppresses the pulmonary inflammatory response in rats challenged with intrapulmonary endotoxin.
TLDR
The data indicate that the antiinflammatory effects of alcohol seem to be primarily based on the effects of ethanol on the PMNs themselves and not on the generation of certain chemotactic stimuli.
Activation of neutrophils and inhibition of the proinflammatory cytokine response by endogenous granulocyte colony-stimulating factor in murine pneumococcal pneumonia.
TLDR
Treatment of mice with pneumococcal pneumonia with an anti-G-CSF antibody reduced neutrophil counts in lung tissue and diminished CD11b expression on pulmonary neutrophils but increased the lung concentrations of tumor necrosis factor- alpha, interleukin-1 beta, and cytokine-induced neutrophIL chemoattractant.
Granulocyte colony-stimulating factor exacerbates acute lung injury induced by intratracheal endotoxin in guinea pigs.
TLDR
Pretreatment with rG-CSF increased sequestration of neutrophils into the lung and exacerbated the lung injury induced by intratracheal endotoxin in CPA-treated guinea pigs.
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