Linked Life Data

17196632

Source:http://linkedlifedata.com/resource/pubmed/id/17196632

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-4-20
pubmed:abstractText
A major cause of the high morbidity and mortality associated with measles infection is attributed to virus-mediated immunosuppression. In this report, we present evidence for a novel strategy of immunosuppression by the measles virus. We observed a marked suppression of lipopolysaccharide (LPS)-induced IL-8, RANTES, TNF-alpha and IL-6 production and NF-kappaB activation in human monocytic cell lines persistently infected with measles virus. This effect was not observed in human epithelial cells lines persistently infected with measles virus. There were no significant differences in expression levels of Toll-like receptors (TLRs) and their associated molecules, or other intracellular signaling molecules of the NF-kappaB signaling pathway in measles-virus-infected monocytic cells compared to uninfected cells. Infected monocytic cells exhibited decreased LPS-induced DNA binding of NF-kappaB and phosphorylation of JNK, namely activation of transcription factors NF-kappaB and AP-1. NF-kappaB was constitutively activated in human epithelial cells persistently infected with measles virus, and LPS treatment resulted in further activation. The cell-type-specific suppression of NF-kappaB activation represents a potential strategy of escape from the host immune system by measles virus via induced immunological silencing in infected cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0042-6822
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
361
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
294-303
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Suppression of NF-kappaB and AP-1 activation in monocytic cells persistently infected with measles virus.
pubmed:affiliation
Department of Microbiology, Sapporo Medical University School of Medicine, South-1, West-17, Chuo-ku, Sapporo 060-8556, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't