Granulocyte colony-stimulating factor modulates the pulmonary host response to endotoxin in the absence and presence of acute ethanol intoxication

Alcohol impairs neutrophil function and predisposes the host to infectious complications. Granulocyte colony-stimulating factor (G-CSF) increases both the number and functional activities of neutrophils, This study investigat ed the effects of G-CSF on the pulmonary response to endotoxin in rats with or without acute ethanol intoxication. Acute ethanol intoxication inhibite d tumor necrosis factor (TNF)-alpha and macrophage inflammatory protein (MI P)-2 production in the lung and suppressed the recruitment of neutrophils i nto the lung. Ethanol also inhibited CD 11b/c expression on recruited neutr ophils and suppressed the phagocytic activity of circulating neutrophils. G -CSF pretreatment up-regulated CD 11b/c expression on circulating polymorph onuclear leukocytes, augmented the recruitment of neutrophils into the lung , and enhanced the phagocytic activity of circulating and recruited neutrop hils in both the absence and presence of acute ethanol intoxication. G-CSF inhibited MIP-2 but not TNF-alpha production in the lung. These data sugges t that G-CSF may be useful in the prevention or treatment of infections in persons immunocompromised by alcohol.