Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-3-6
pubmed:abstractText
Respiratory syncytial virus (RSV) is a leading cause of bronchiolitis in young children. Microbial agents such as endotoxin and RSV are implicated in airway inflammation during the development of reactive airway disease (RAD) later in childhood. Toll-like receptors (TLRs) are involved in an inflammation cascade through pathogen-associated molecular pattern recognition including lipopolysaccharide (LPS) and viral components. In this study, we investigated the expression of TLRs and cytokine-chemokine production profiles of RSV-infected epithelial cells. In live-RSV infected human tracheal epithelial cell line (9HTEo), TLRs 1-10 mRNA levels were up-regulated in a time-dependent manner compared with ultraviolet (UV)-inactivated RSV. RSV was shown to alter TLR4 membrane and cytosolic location in epithelial cells. Stimulating RSV-infected epithelial cells with TLR4 agonist LPS increased synthesis of IL-6, IL-8, and reduced regulated on activation, normal T cell expressed and secreted (RANTES) production. TLR4 neutralizing antibody HTA125 and TLR4-targeting RNA interference experiments revealed that TLR4 signaling pathway played a predominant role in mediating LPS-induced-IL-6 production of RSV infected epithelial cells. Altogether, our studies indicated that TLR4 play a critical role in leading LPS mediated-IL-6 response in RSV infected-epithelial cells and might be an important factor influencing the cytokine-chemokine profile of epithelial cells interacting with virus and endotoxin, which is correlated with phenotypes of RSV diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, http://linkedlifedata.com/resource/pubmed/chemical/CCL5 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL5, http://linkedlifedata.com/resource/pubmed/chemical/IL6 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/IL8 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-8, http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering, http://linkedlifedata.com/resource/pubmed/chemical/TLR4 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 4, http://linkedlifedata.com/resource/pubmed/chemical/lipopolysaccharide, Escherichia...
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1530-0447
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
65
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
156-62
pubmed:meshHeading
pubmed-meshheading:18948841-Antibodies, pubmed-meshheading:18948841-Cell Line, pubmed-meshheading:18948841-Chemokine CCL5, pubmed-meshheading:18948841-Epithelial Cells, pubmed-meshheading:18948841-Humans, pubmed-meshheading:18948841-Interleukin-6, pubmed-meshheading:18948841-Interleukin-8, pubmed-meshheading:18948841-Lipopolysaccharides, pubmed-meshheading:18948841-Protein Transport, pubmed-meshheading:18948841-RNA, Messenger, pubmed-meshheading:18948841-RNA, Small Interfering, pubmed-meshheading:18948841-RNA Interference, pubmed-meshheading:18948841-Respiratory Syncytial Virus, Human, pubmed-meshheading:18948841-Signal Transduction, pubmed-meshheading:18948841-Time Factors, pubmed-meshheading:18948841-Toll-Like Receptor 4, pubmed-meshheading:18948841-Trachea, pubmed-meshheading:18948841-Up-Regulation
pubmed:year
2009
pubmed:articleTitle
Lipopolysaccharide induces IL-6 production in respiratory syncytial virus-infected airway epithelial cells through the toll-like receptor 4 signaling pathway.
pubmed:affiliation
Immunological Laboratory of Children Research Center, Children's Hospital of Chongqing Medical University, Chongqing 400014, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't