Linked Life Data

19556613

Source:http://linkedlifedata.com/resource/pubmed/id/19556613

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-8-31
pubmed:abstractText
Infection with the enteric pathogen enterohemorrhagic Escherichia coli (EHEC) causes a variety of symptoms ranging from nonbloody diarrhea to more severe sequelae including hemorrhagic colitis, altered sensorium and seizures, and even life-threatening complications, such as hemolytic uremic syndrome and thrombotic thrombocytopenic purpura. The more severe consequences of EHEC infection are attributable to the production of Shiga toxin (Stx) and its subsequent effects on the vasculature, which expresses high levels of the Stx receptor, Gb3. Interestingly, the intestinal epithelium does not express Gb3. Despite the lack of Gb3 receptor expression, intestinal epithelial cells translocate Stx. The effect of Stx on intestinal epithelial cells is controversial with some studies demonstrating induction of inflammation and others not. This may be difficult to resolve because EHEC expresses both proinflammatory molecules, such as flagellin, and factor(s) that dampen the inflammatory response of epithelial cells. The goal of our study was to define the effect of Stx on the inflammatory response of intestinal epithelial cells and to determine whether infection by EHEC modulates this response. Here we show that Stx is a potent inducer of the inflammatory response in intestinal epithelial cells and confirm that EHEC attenuates the induction of IL-8 by host-derived proinflammatory cytokines. More importantly, however, we show that infection with EHEC attenuates the inflammatory response by intestinal epithelial cells to its own toxin. We speculate that the ability of EHEC to dampen epithelial cell inflammatory responses to Stx and cytokines facilitates intestinal colonization.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1522-1547
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
297
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
G576-81
pubmed:dateRevised
2010-9-2
pubmed:meshHeading
pubmed-meshheading:19556613-Cytokines, pubmed-meshheading:19556613-Enteritis, pubmed-meshheading:19556613-Enterohemorrhagic Escherichia coli, pubmed-meshheading:19556613-Epithelial Cells, pubmed-meshheading:19556613-Escherichia coli Infections, pubmed-meshheading:19556613-HT29 Cells, pubmed-meshheading:19556613-Host-Pathogen Interactions, pubmed-meshheading:19556613-Humans, pubmed-meshheading:19556613-I-kappa B Proteins, pubmed-meshheading:19556613-Inflammation Mediators, pubmed-meshheading:19556613-Interleukin-1beta, pubmed-meshheading:19556613-Interleukin-8, pubmed-meshheading:19556613-Intestinal Mucosa, pubmed-meshheading:19556613-Protein Transport, pubmed-meshheading:19556613-Shiga Toxins, pubmed-meshheading:19556613-Trihexosylceramides, pubmed-meshheading:19556613-Tumor Necrosis Factor-alpha
pubmed:year
2009
pubmed:articleTitle
Enterohemorrhagic Escherichia coli suppresses inflammatory response to cytokines and its own toxin.
pubmed:affiliation
Department of Medicine, Section of Digestive Diseases and Nutrition, University of Illinois and Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois 60612-7323, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, N.I.H., Extramural