title: Modulation of the lung host response by granulocyte colony-stimulating factor in rats challenged with intrapulmonary endotoxin.
abstract: The effects of granulocyte colony-stimulating factor (G-CSF) on the functional activities of circulating and lung-recruited neutrophils (PMNs) and alveolar macrophages (AMs) were studied in rats to further elucidate the mechanisms underlying G-CSF-enhanced pulmonary host defense. Animals received G-CSF or vehicle twice a day for 2 days, followed by an intratracheal challenge with endotoxin or saline. G-CSF up-regulated CD11b/c expression and mean channel fluorescence intensity of phagocytosis in circulating PMNs. G-CSF also enhanced phagocytic activities, reflected by both the percentage of phagocytosis and mean channel fluorescence intensity in lung-recruited PMNs and AMs in intratracheal endotoxin-challenged rats. The endotoxin-induced increase in pulmonary production of tumor necrosis factor-alpha and cytokine-induced neutrophil chemoattractant was not affected by G-CSF pretreatment. These data demonstrate that G-CSF-enhanced pulmonary recruitment of PMNs is primarily based on the effects of G-CSF on the PMNs themselves, rather than the generation of certain chemotactic stimuli, i.e., cytokine-induced neutrophil chemoattractant and tumor necrosis factor-alpha. The enhanced phagocytic activities of lung-recruited PMNs and AMs also augment pulmonary host defenses in G-CSF-pretreated animals.
authors.affiliation: Department of Medicine, Louisiana State University Medical Center, New Orleans 70112, USA.
authors.forename: P
authors.initials: P
authors.lastname: Zhang
authors.forename: G J
authors.initials: GJ
authors.lastname: Bagby
authors.forename: D A
authors.initials: DA
authors.lastname: Stoltz
authors.forename: J A
authors.initials: JA
authors.lastname: Spitzer
authors.forename: W R
authors.initials: WR
authors.lastname: Summer
authors.forename: S
authors.initials: S
authors.lastname: Nelson
mesh_terms: D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D018821:CD18 Antigens / Q000276:immunology / Q000378:metabolism; D019743:Chemokines, CXC; D002630:Chemotactic Factors / Q000276:immunology / Q000378:metabolism; D004731:Endotoxins / Q000276:immunology* / Q000502:physiology; D016179:Granulocyte Colony-Stimulating Factor / Q000276:immunology* / Q000502:physiology; D006133:Growth Substances / Q000276:immunology / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000276:immunology / Q000378:metabolism; D007111:Immunity, Cellular / Q000276:immunology* / Q000502:physiology; D016167:Integrin alphaXbeta2 / Q000276:immunology / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins; D008168:Lung / Q000166:cytology* / Q000276:immunology / Q000502:physiology; D016177:Macrophage-1 Antigen / Q000276:immunology / Q000378:metabolism; D016676:Macrophages, Alveolar / Q000276:immunology / Q000502:physiology; D008297:Male; D009504:Neutrophils / Q000276:immunology / Q000502:physiology; D010587:Phagocytosis / Q000276:immunology / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000378:metabolism
chemical_list: D018821:CD18 Antigens; D019743:Chemokines, CXC; D002630:Chemotactic Factors; D004731:Endotoxins; D006133:Growth Substances; D016167:Integrin alphaXbeta2; D036341:Intercellular Signaling Peptides and Proteins; D016177:Macrophage-1 Antigen; D014409:Tumor Necrosis Factor-alpha; D016179:Granulocyte Colony-Stimulating Factor; D006861:Hydrogen Peroxide