Linked Life Data

17191166

Source:http://linkedlifedata.com/resource/pubmed/id/17191166

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-12-27
pubmed:abstractText
As a step toward understanding the role played by host gene expression in the development and pathogenesis of persistent Chlamydia pneumoniae infection, modulation of the host-cell transcriptional response during interferon (IFN)- gamma -induced persistent C. pneumoniae infection of HL cells was examined by a cDNA array and then selectively by a real-time quantitative reverse transcription-polymerase chain reaction. We identified 9 host cell genes whose transcription was consistently altered during IFN- gamma -induced persistent C. pneumoniae infection. The strongest up-regulation of persistent infection, compared with controls (active infection and IFN- gamma ) was identified for insulin-like growth factor-binding protein 6, IFN-stimulated protein 15 kDa, cyclin D1, and interleukin-7 receptor genes. These results suggest that, during persistent infection, C. pneumoniae reprograms the host transcriptional machinery that regulates a variety of cellular processes, including adhesion, regulation of the cell cycle, growth, and inflammatory response, all of which might play important roles in the pathogenesis of persistent C. pneumoniae infection.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-1899
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
195
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
212-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Up-regulation of host cell genes during interferon-gamma-induced persistent Chlamydia pneumoniae infection in HL cells.
pubmed:affiliation
Haartman Institute, Department of Virology, University of Helsinki, Helsinki, Finland. laura.mannonen@helsinki.fi
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't