Linked Life Data

19538320

Source:http://linkedlifedata.com/resource/pubmed/id/19538320

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2009-6-22
pubmed:abstractText
To date, the precise etiology of inflammatory bowel disease (IBD) remains largely unknown; however, it is well accepted that IBD results from a dysregulated mucosal immune response to environmental factors in genetically susceptible hosts. The primary defect, in at least a subpopulation of IBD patients, may be due to abnormal intestinal epithelial barrier function. The SAMP1/YitFc (SAMP) mouse strain is a spontaneous model of IBD, closely resembling Crohn's disease for its histologic features and localization to the terminal ileum. Dysregulated epithelial barrier function that precedes histologic evidence of ileitis has been reported to be the primary defect in SAMP mice. Data suggest that barrier dysfunction occurs in the absence of commensal bacteria and is accompanied by aberrant expression of the tight junction proteins claudin-2 and occludin. Further investigation is needed to define the precise role of the intestinal epithelium, as well as the apical junctional complex and its associated proteins, in the pathogenesis of IBD in order to determine the etiology and aid in the development of novel treatment modalities for these devastating diseases.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1749-6632
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
1165
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
301-7
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Mechanisms of tight junction dysregulation in the SAMP1/YitFc model of Crohn's disease-like ileitis.
pubmed:affiliation
Department of Medicine, Division of Gastroenterology & Hepatology, University of Virginia, Charlottesville, VA 22908, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural