Modulation of the lung host response by granulocyte colony-stimulating factor in rats challenged with intrapulmonary endotoxin

Shock. 1997 Mar;7(3):193-9. doi: 10.1097/00024382-199703000-00007.

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Bronchoalveolar Lavage Fluid / chemistry
  • CD18 Antigens / immunology
  • CD18 Antigens / metabolism
  • Chemokines, CXC*
  • Chemotactic Factors / immunology
  • Chemotactic Factors / metabolism
  • Endotoxins / immunology*
  • Endotoxins / physiology
  • Granulocyte Colony-Stimulating Factor / immunology*
  • Granulocyte Colony-Stimulating Factor / physiology
  • Growth Substances / immunology
  • Growth Substances / metabolism
  • Hydrogen Peroxide / immunology
  • Hydrogen Peroxide / metabolism
  • Immunity, Cellular / immunology*
  • Immunity, Cellular / physiology
  • Integrin alphaXbeta2 / immunology
  • Integrin alphaXbeta2 / metabolism
  • Intercellular Signaling Peptides and Proteins*
  • Lung / cytology*
  • Lung / immunology
  • Lung / physiology
  • Macrophage-1 Antigen / immunology
  • Macrophage-1 Antigen / metabolism
  • Macrophages, Alveolar / immunology
  • Macrophages, Alveolar / physiology
  • Male
  • Neutrophils / immunology
  • Neutrophils / physiology
  • Phagocytosis / immunology
  • Phagocytosis / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Time Factors
  • Tumor Necrosis Factor-alpha / immunology
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • CD18 Antigens
  • Chemokines, CXC
  • Chemotactic Factors
  • Endotoxins
  • Growth Substances
  • Integrin alphaXbeta2
  • Intercellular Signaling Peptides and Proteins
  • Macrophage-1 Antigen
  • Tumor Necrosis Factor-alpha
  • Granulocyte Colony-Stimulating Factor
  • Hydrogen Peroxide