Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-8-29
pubmed:abstractText
We previously reported that IL-1beta and the decoy receptor for IL-1 (IL-1RII) are expressed by intestinal epithelial cells (IEC) during detachment-induced cell death, or "anoikis." We now investigated whether IL-1 regulates anoikis. Skewing the balance in favor of IL-1, by blocking IL-1RII or by adding IL-1beta to detached rat IEC-18 cells, reduced cell death. The protective effect of anti-IL-1RII was reversed by blocking IL-1beta, confirming the anti-apoptotic effect was due to endogenous IL-1beta. Added IL-1beta also rescued cells from anoikis and was associated with considerable aggregation of the detached cells. Aggregate formation and the anti-apoptotic effect of added IL-1beta were prevented by blocking E-cadherin, indicating that IL-1 promoted aggregation and indirectly, survival. On the other hand, treating detached cells with IL-1beta and an anti-beta(1) integrin antibody abolished the protective effect of IL-1beta but not the aggregates. We conclude that the anti-apoptotic effect of IL-1 is mediated through a beta(1) integrin-dependent event secondary to cell-cell adhesion. This illustrates a previously uncharacterized role for IL-1 in the intestine wherein this cytokine may facilitate the preservation of the epithelial monolayer integrity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0014-4827
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Academic Press.
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
269
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
109-16
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Endogenous IL-1 and type II IL-1 receptor expression modulate anoikis in intestinal epithelial cells.
pubmed:affiliation
Department of Microbiology, Dalhousie University, Halifax, Nova Scotia, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't