Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1997-2-27
pubmed:abstractText
Previous studies have shown that C. pneumoniae is able to infect human endothelial cells in vitro. In this report, the ability of C. pneumoniae to induce the expression of E-selectin or endothelial-leukocyte adhesion molecule 1 (ELAM-1), intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) on human umbilical vein endothelial (HUVE) cell surface was investigated. C. pneumoniae was found to cause a moderate upregulation of the adhesion molecules. Maximal expression of E-selectin was noted at 6 h post infection (p.i.) and that of ICAM-1 and VCAM-1 at 20 h p.i. The capability of C. pneumoniae to grow in endothelial cells and to stimulate the expression of adhesion molecules essential for leukocyte-endothelial cell interactions suggests a role for C. pneumoniae as a local pathogenetic factor in vascular inflammatory alterations, including atherogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0882-4010
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
407-11
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Expression of adhesion molecules on endothelial cells stimulated by Chlamydia pneumoniae.
pubmed:affiliation
Department of Virology, University of Helsinki, Finland.
pubmed:publicationType
Journal Article