title: The potential of various lipopolysaccharides to release monocyte chemotactic activity from lung epithelial cells and fibroblasts.
abstract: Although the cytotoxicity of lipopolysaccharide (LPS) derived from Pseudomonas aeruginosa, i.e. Limulus amoebocyte lysate activity, is less potent than that from Escherichia coli 0127:B8, P. aeruginosa induces prominent sustained lung inflammation, as in cystic fibrosis. The present study was designed to examine the potential for several LPSs obtained from E. coli and P. aeruginosa to release monocyte chemotactic activity (MCA) from lung cells. LPSs differentially stimulated A549 cells, BEAS-2B cells and lung fibroblasts to release MCA (P. aeruginosa >E. coli 0127:B8 from Difco >055:B5 from Sigma >026:B6 (Sigma)). E. coli 0127:B8 (Sigma) and 0111:B4 (Sigma) did not stimulate these cells. MCA was determined by means of checkerboard analysis. Molecular sieve column chromatography revealed four chemotactic peaks. The release of MCA was inhibited by cycloheximide and lipoxygenase inhibitors. Experiments with blocking antibodies suggested that much of the MCA was secondary to monocyte chemoattractant protein-1 (MCP-1) and granulocyte-macrophage colony-stimulating factor (GM-CSF). Thus, the concentrations of these chemoattractants were examined and it was found that the potency of the various LPSs to stimulate MCA closely paralleled their potency in releasing MCP-1 and GM-GSF. Serum augmented the release of MCP-1 and GM-CSF. However, the differences among LPSs from E. coli and P. aeruginosa in stimulating A549 cells were observed. These data suggest that Pseudomonas aeruginosa lipopolysaccharide may stimulate lung cells to release more monocyte chemotactic activity than lipopolysaccharides derived from Escherichia coli, leading to sustained prominent lung inflammation.
authors.affiliation: The First Dept of Internal Medicine, Shinshu University, School of Medicine, Matsumoto, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Koyama
authors.forename: E
authors.initials: E
authors.lastname: Sato
authors.forename: H
authors.initials: H
authors.lastname: Nomura
authors.forename: K
authors.initials: K
authors.lastname: Kubo
authors.forename: M
authors.initials: M
authors.lastname: Miura
authors.forename: T
authors.initials: T
authors.lastname: Yamashita
authors.forename: S
authors.initials: S
authors.lastname: Nagai
authors.forename: T
authors.initials: T
authors.lastname: Izumi
mesh_terms: D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000378:metabolism; D002634:Chemotaxis, Leukocyte / Q000502:physiology*; D003513:Cycloheximide / Q000494:pharmacology; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D004926:Escherichia coli; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000378:metabolism; D006801:Humans; D007975:Leukotriene B4 / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology*; D016859:Lipoxygenase Inhibitors / Q000494:pharmacology; D008168:Lung / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D009000:Monocytes / Q000502:physiology*; D010972:Platelet Activating Factor / Q000037:antagonists & inhibitors; D010980:Platelet Membrane Glycoproteins / Q000037:antagonists & inhibitors; D011112:Polymyxin B / Q000494:pharmacology; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D011550:Pseudomonas aeruginosa; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled
chemical_list: D018932:Chemokine CCL2; D008070:Lipopolysaccharides; D016859:Lipoxygenase Inhibitors; D010972:Platelet Activating Factor; D010980:Platelet Membrane Glycoproteins; D011500:Protein Synthesis Inhibitors; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; C039351:platelet activating factor receptor; D007975:Leukotriene B4; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D003513:Cycloheximide; D011112:Polymyxin B