Linked Life Data

15109931

Source:http://linkedlifedata.com/resource/pubmed/id/15109931

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-4-27
pubmed:abstractText
Human bronchial epithelial cell pro-inflammatory molecule expression plays a role in the pathogenesis of airway diseases. We hypothesize that Yersinia outer protein-J (YopJ), a Yersinia virulence effector which inhibits mitogen activated protein (MAP) kinase kinases (MKKs), attenuates epithelial cell pro-inflammatory molecule expression. 16HBE14o-cells were co-transfected with cDNAs encoding Yersinia pseudotuberculosis YopJ or empty vector. Expression of YopJ reduced activation of extracellular signal regulated kinase (ERK)-2, Jun amino terminal kinase (JNK)-1 and IkappaB kinase (IKK)-beta. YopJ also blocked transactivation of NF-kappaB and AP-1 promoter sequences which has been shown to regulate chemokine expression. Finally, expression of YopJ reduced transcription from the IL-8, RANTES (regulated upon activation, normal T cell expressed and secreted) and intercellular adhesion molecule (ICAM)-1 promoters. We conclude that YopJ expression blocks the innate immune response in lung epithelial cells, the site of Yersinia pestis infection. Inhibition of bronchial epithelial cell responses by YopJ is consistent with the notion that MAP kinases regulates bronchial epithelial cell pro-inflammatory molecule expression.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1569-9048
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
140
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
89-97
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Yersinia YopJ inhibits pro-inflammatory molecule expression in human bronchial epithelial cells.
pubmed:affiliation
Department of Pediatrics, University of Chicago, Chicago, IL 60637-1470, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't