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Endogenous IL-1 and type II IL-1 receptor expression modulate anoikis in intestinal epithelial cells
C C Waterhouse1, R R Joseph, A W Stadnyk
1Department of Microbiology, Dalhousie University, Halifax, Nova Scotia, Canada.
Experimental Cell Research
|August 30, 2001
Summary
Interleukin-1 (IL-1) protects intestinal epithelial cells from anoikis, a form of cell death. IL-1 promotes cell-cell adhesion and survival through beta(1) integrin signaling, maintaining gut barrier integrity.
Area of Science:
- Cell Biology
- Immunology
- Gastroenterology
Background:
- Intestinal epithelial cells (IECs) undergo anoikis upon detachment.
- Interleukin-1beta (IL-1beta) and its decoy receptor (IL-1RII) are expressed by IECs during anoikis.
Purpose of the Study:
- To investigate the role of IL-1 in regulating anoikis in IECs.
- To elucidate the molecular mechanisms by which IL-1 influences cell survival and intestinal barrier integrity.
Main Methods:
- Detached rat IEC-18 cells were treated with IL-1beta, anti-IL-1RII antibodies, anti-beta(1) integrin antibodies, or anti-E-cadherin antibodies.
- Cell death (anoikis), cell aggregation, and signaling pathways were analyzed.
Main Results:
- Blocking IL-1RII or adding IL-1beta reduced anoikis in detached IECs.
- IL-1beta promoted cell-cell aggregation via E-cadherin, which was essential for its anti-apoptotic effect.
- The protective effect of IL-1beta was dependent on beta(1) integrin signaling, secondary to cell adhesion.
Conclusions:
- IL-1 plays a novel role in promoting intestinal epithelial cell survival by enhancing cell-cell adhesion and activating beta(1) integrin-dependent pathways.
- This cytokine-mediated mechanism may preserve the integrity of the intestinal epithelial monolayer.