Linked Life Data

16113820

Source:http://linkedlifedata.com/resource/pubmed/id/16113820

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-8-22
pubmed:abstractText
Microvascular endothelial damage underlies the pathological changes in haemorrhagic colitis and the haemolytic uraemic syndrome (HUS) caused by enterohaemorrhagic Escherichia coli (EHEC). Shiga toxins (Stxs) are presently the best characterised EHEC virulence factors that can cause the microvascular endothelium injury. Stxs are released by EHEC in the intestine, absorbed across the gut epithelium into the circulation, and transported to small vessel endothelial cells. Then, they presumably injure the host cell by inhibiting protein synthesis, stimulating prothrombotic messages, or inducing apoptosis. The net result is a multi-organ thrombotic process. Moreover, Stxs stimulate a variety of non-endothelial cells to produce and secrete inflammatory mediators (cytokines, chemokines, adhesion molecules) which could potentiate the effects of Stxs on endothelial cells. The association of HUS with Stx-negative E. coli strains stimulated intensive research on putative non-Stx virulence factors, which might also contribute to the pathogenesis of HUS and haemorrhagic colitis. Based on current data, cytolethal distending toxin, EHEC haemolysin, and subtilase cytotoxin might be such candidates.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0340-6245
pubmed:author
pubmed:issnType
Print
pubmed:volume
94
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
312-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Consequences of enterohaemorrhagic Escherichia coli infection for the vascular endothelium.
pubmed:affiliation
Institute for Hygiene and National Consulting Laboratory on Haemolytic Uraemic Syndrome, University Hospital Münster, Germany.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't