Linked Life Data

10570304

Source:http://linkedlifedata.com/resource/pubmed/id/10570304

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1999-12-20
pubmed:abstractText
Cell adhesion molecule expression (CAM) and IL-8 release in lung microvascular endothelium facilitate neutrophil accumulation in the lung. This study investigated the effects of lipoteichoic acid (LTA), a cell wall component of Gram-positive bacteria, alone and with LPS or TNF-alpha, on CAM expression and IL-8 release in human lung microvascular endothelial cells (HLMVEC). The concentration-dependent effects of Staphylococcus aureus (S. aureus) LTA (0.3-30 microg/ml) on ICAM-1 and E-selectin expression and IL-8 release were bell shaped. Streptococcus pyogenes (S. pyogenes) LTA had no effect on CAM expression, but caused a concentration-dependent increase in IL-8 release. S. aureus and S. pyogenes LTA (30 microg/ml) abolished LPS-induced CAM expression, and S. aureus LTA reduced LPS-induced IL-8 release. In contrast, the effects of S. aureus LTA with TNF-alpha on CAM expression and IL-8 release were additive. Inhibitory effects of LTA were not due to decreased HLMVEC viability, as assessed by ethidium homodimer-1 uptake. Changes in neutrophil adhesion to HLMVEC paralleled changes in CAM expression. Using RT-PCR to assess mRNA levels, S. aureus LTA (3 microg/ml) caused a protein synthesis-dependent reduction (75%) in LPS-induced IL-8 mRNA and decreased the IL-8 mRNA half-life from >6 h with LPS to approximately 2 h. These results suggest that mechanisms exist to prevent excessive endothelial cell activation in the presence of high concentrations of bacterial products. However, inhibition of HLMVEC CAM expression and IL-8 release ultimately may contribute to decreased neutrophil accumulation, persistence of bacteria in the lung, and increased severity of infection.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
163
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6139-47
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10570304-Cell Adhesion Molecules, pubmed-meshheading:10570304-Drug Interactions, pubmed-meshheading:10570304-E-Selectin, pubmed-meshheading:10570304-Endothelium, Vascular, pubmed-meshheading:10570304-Half-Life, pubmed-meshheading:10570304-Humans, pubmed-meshheading:10570304-Intercellular Adhesion Molecule-1, pubmed-meshheading:10570304-Interleukin-8, pubmed-meshheading:10570304-Lipopolysaccharides, pubmed-meshheading:10570304-Lung, pubmed-meshheading:10570304-Lung Diseases, pubmed-meshheading:10570304-Microcirculation, pubmed-meshheading:10570304-Neutrophil Infiltration, pubmed-meshheading:10570304-RNA, Messenger, pubmed-meshheading:10570304-RNA Stability, pubmed-meshheading:10570304-Sepsis, pubmed-meshheading:10570304-Streptococcus, pubmed-meshheading:10570304-Streptococcus pyogenes, pubmed-meshheading:10570304-Teichoic Acids, pubmed-meshheading:10570304-Tumor Necrosis Factor-alpha
pubmed:year
1999
pubmed:articleTitle
Lipoteichoic acid inhibits lipopolysaccharide-induced adhesion molecule expression and IL-8 release in human lung microvascular endothelial cells.
pubmed:affiliation
Applied Pharmacology and Unit of Critical Care, National Heart and Lung Institute Division, Imperial College School of Medicine, London, United Kingdom.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't