Linked Life Data

19632896

Source:http://linkedlifedata.com/resource/pubmed/id/19632896

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2009-11-25
pubmed:abstractText
The intestinal epithelium restricts free passage of toxic and infectious molecules from the gut lumen while allowing selective paracellular absorption across the tight junction. Inflammatory bowel disease (IBD) patients demonstrate a loss of tight junction barrier function, increased pro-inflammatory cytokine production, and immune dysregulation; however, the relationship between these events is incompletely understood. Although tight junction barrier defects are insufficient to cause experimental IBD, mucosal immune activation is altered in response to increased epithelial permeability. Thus, an evolving model suggests that barrier dysfunction may predispose or enhance disease progression and therapies targeted to specifically restore the barrier function may provide an alternative or supplement to immunology-based therapies.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1471-4973
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
715-20
pubmed:dateRevised
2011-5-17
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
The tight junction in inflammatory disease: communication breakdown.
pubmed:affiliation
Department of Pathology, The University of Chicago, Chicago, IL 60637, USA.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural