PMID- 10543273
OWN - NLM
STAT- MEDLINE
DCOM- 19991202
LR  - 20190822
IS  - 0903-1936 (Print)
IS  - 0903-1936 (Linking)
VI  - 14
IP  - 3
DP  - 1999 Sep
TI  - The potential of various lipopolysaccharides to release monocyte chemotactic 
      activity from lung epithelial cells and fibroblasts.
PG  - 545-52
AB  - 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.
FAU - Koyama, S
AU  - Koyama S
AD  - The First Dept of Internal Medicine, Shinshu University, School of Medicine, 
      Matsumoto, Japan.
FAU - Sato, E
AU  - Sato E
FAU - Nomura, H
AU  - Nomura H
FAU - Kubo, K
AU  - Kubo K
FAU - Miura, M
AU  - Miura M
FAU - Yamashita, T
AU  - Yamashita T
FAU - Nagai, S
AU  - Nagai S
FAU - Izumi, T
AU  - Izumi T
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - England
TA  - Eur Respir J
JT  - The European respiratory journal
JID - 8803460
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Lipoxygenase Inhibitors)
RN  - 0 (Platelet Activating Factor)
RN  - 0 (Platelet Membrane Glycoproteins)
RN  - 0 (Protein Synthesis Inhibitors)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Receptors, G-Protein-Coupled)
RN  - 0 (platelet activating factor receptor)
RN  - 1HGW4DR56D (Leukotriene B4)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
RN  - 98600C0908 (Cycloheximide)
RN  - J2VZ07J96K (Polymyxin B)
SB  - IM
MH  - Cells, Cultured
MH  - Chemokine CCL2/metabolism
MH  - Chemotaxis, Leukocyte/*physiology
MH  - Cycloheximide/pharmacology
MH  - Epithelial Cells/drug effects/metabolism
MH  - *Escherichia coli
MH  - Fibroblasts/drug effects/metabolism
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/metabolism
MH  - Humans
MH  - Leukotriene B4/pharmacology
MH  - Lipopolysaccharides/*pharmacology
MH  - Lipoxygenase Inhibitors/pharmacology
MH  - Lung/cytology/*drug effects/metabolism
MH  - Monocytes/*physiology
MH  - Platelet Activating Factor/antagonists & inhibitors
MH  - Platelet Membrane Glycoproteins/antagonists & inhibitors
MH  - Polymyxin B/pharmacology
MH  - Protein Synthesis Inhibitors/pharmacology
MH  - *Pseudomonas aeruginosa
MH  - *Receptors, Cell Surface
MH  - *Receptors, G-Protein-Coupled
EDAT- 1999/10/30 00:00
MHDA- 1999/10/30 00:01
CRDT- 1999/10/30 00:00
PHST- 1999/10/30 00:00 [pubmed]
PHST- 1999/10/30 00:01 [medline]
PHST- 1999/10/30 00:00 [entrez]
AID - 10.1034/j.1399-3003.1999.14c11.x [doi]
PST - ppublish
SO  - Eur Respir J. 1999 Sep;14(3):545-52. doi: 10.1034/j.1399-3003.1999.14c11.x.