Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
52
pubmed:dateCreated
2003-12-22
pubmed:abstractText
Airway epithelial cells are unresponsive to endotoxin (lipopolysaccharide (LPS)) exposure under normal conditions. This study demonstrates that respiratory syncytial virus (RSV) infection results in increased sensitivity to this environmental exposure. Infection with RSV results in increased expression of Toll-like receptor (TLR) 4 mRNA, protein, and increased TLR4 membrane localization. This permits significantly enhanced LPS binding to the epithelial monolayer that is blocked by disruption of the Golgi. The increased TLR4 results in an LPS-induced inflammatory response as demonstrated by increased mitogen-activated protein (MAP) kinase activity, IL-8 production, and tumor necrosis factor alpha production. RSV infection also allowed for tumor necrosis factor alpha production subsequent to TLR4 cross-linking with an immobilized antibody. These data suggest that RSV infection sensitizes airway epithelium to a subsequent environmental exposure (LPS) by altered expression and membrane localization of TLR4. The increased interaction between airway epithelial cells and LPS has the potential to profoundly alter airway inflammation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
26
pubmed:volume
278
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
53035-44
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:14565959-Blotting, Western, pubmed-meshheading:14565959-Cell Line, Tumor, pubmed-meshheading:14565959-Cell Membrane, pubmed-meshheading:14565959-Cell Separation, pubmed-meshheading:14565959-Cells, Cultured, pubmed-meshheading:14565959-Cross-Linking Reagents, pubmed-meshheading:14565959-Dose-Response Relationship, Drug, pubmed-meshheading:14565959-Endotoxins, pubmed-meshheading:14565959-Epithelial Cells, pubmed-meshheading:14565959-Epithelium, pubmed-meshheading:14565959-Flow Cytometry, pubmed-meshheading:14565959-Golgi Apparatus, pubmed-meshheading:14565959-HeLa Cells, pubmed-meshheading:14565959-Humans, pubmed-meshheading:14565959-Inflammation, pubmed-meshheading:14565959-Interleukin-8, pubmed-meshheading:14565959-Lipopolysaccharides, pubmed-meshheading:14565959-Lung, pubmed-meshheading:14565959-MAP Kinase Signaling System, pubmed-meshheading:14565959-Macrophages, Alveolar, pubmed-meshheading:14565959-Membrane Glycoproteins, pubmed-meshheading:14565959-Microscopy, Confocal, pubmed-meshheading:14565959-Microscopy, Fluorescence, pubmed-meshheading:14565959-Models, Biological, pubmed-meshheading:14565959-Monocytes, pubmed-meshheading:14565959-RNA, Messenger, pubmed-meshheading:14565959-Receptors, Cell Surface, pubmed-meshheading:14565959-Respiratory Syncytial Viruses, pubmed-meshheading:14565959-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:14565959-Time Factors, pubmed-meshheading:14565959-Toll-Like Receptor 4, pubmed-meshheading:14565959-Toll-Like Receptors, pubmed-meshheading:14565959-Tumor Necrosis Factor-alpha, pubmed-meshheading:14565959-Up-Regulation
pubmed:year
2003
pubmed:articleTitle
Respiratory syncytial virus up-regulates TLR4 and sensitizes airway epithelial cells to endotoxin.
pubmed:affiliation
University of Iowa Roy J. and Lucille A. Carver College of Medicine and Veterans Affairs Medical Center, Iowa City, Iowa 52240, USA. martha-monick@uiowa.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.