title: The potential of various lipopolysaccharides to release IL-8 and G-CSF.
abstract: Lipopolysaccharide (LPS) derived from Pseudomonas aeruginosa is less cytotoxic than that from Escherichia coli. But P. aeruginosa induces a prominent sustained lung inflammation as in cystic fibrosis and diffuse panbronchiolotis. The present study examined the potential for several LPSs obtained from E. coli and P. aeruginosa to release neutrophil chemotactic activity (NCA) from lung cells. LPSs differently stimulated A549 cells, BEAS-2B cells, and lung fibroblasts to release NCA [P. aeruginosa > E. coli 0127:B8 (Difco) > E. coli 055:B5 (Sigma) > E. coli 026:B6 (Sigma)]. E. coli 0127:B8 (Sigma) and 0111:B4 (Sigma) did not stimulate these cells. NCA was chemotactic by checkerboard analysis. Molecular-sieve column chromatography revealed three chemotactic peaks. The release of NCA was inhibited by cycloheximide and lipoxygenase inhibitors. Experiments with blocking antibodies suggested that much of the NCA was secondary to the release of interleukin (IL)-8 and granulocyte colony-stimulating factor (G-CSF). Thus we examined the concentrations of IL-8 and G-CSF and found that the potency of the various LPSs to stimulate NCA closely paralleled the potency in releasing IL-8 and G-CSF. But a difference among LPSs to stimulate A549 cells was observed. Finally, the release of IL-6 showed similar results. These data suggest that P. aeruginosa LPS may stimulate lung cells to release more NCA than E. coli LPSs, leading to sustained lung inflammation.
authors.affiliation: National Chuushin Matsumoto Hospital, Matsumoto 399, 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: D000906:Antibodies / Q000494:pharmacology; D002460:Cell Line; D004926:Escherichia coli; D016179:Granulocyte Colony-Stimulating Factor / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000276:immunology / Q000378:metabolism*; D007975:Leukotriene B4 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D009994:Osmolar Concentration; D010972:Platelet Activating Factor / Q000378:metabolism; D011112:Polymyxin B / Q000494:pharmacology; D011550:Pseudomonas aeruginosa; D018102:Receptors, Leukotriene B4 / Q000037:antagonists & inhibitors
chemical_list: D000906:Antibodies; D015850:Interleukin-6; D016209:Interleukin-8; D008070:Lipopolysaccharides; D010972:Platelet Activating Factor; D018102:Receptors, Leukotriene B4; D016179:Granulocyte Colony-Stimulating Factor; D007975:Leukotriene B4; D011112:Polymyxin B