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Mediators of Inflammation
Volume 11 (2002), Issue 1, Pages 39-45
IL-1 stimulates ceramide accumulation without inducing apoptosis in intestinal epithelial cells
1Department of Physiology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon
2Department of Human Morphology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon
3Department of Pediatrics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon
Copyright © 2002 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Background: In inflammatory bowel disease (IBD), cytokine levels (such as interleukin-1 (IL-1)) are elevated. We have shown previously that IL-1 activates phospholipid signaling pathways in intestinal epithelial cells (IEC), leading to increased ceramide levels.
Aim: To determine whether ceramide induces apoptosis in IEC.
Methods: Apoptosis was evaluated by annexin-Vbinding or Hoechst nuclear staining. Levels of bcl-2, bcl-x, bax, p53 and p21 were determined by Western blotting, and cell cycle analysis was determined by flow cytometry.
Results: IL-1 increased ceramide accumulation in a time-dependent and concentration-dependent manner with a peak response at 4 h, with [IL-1] = 30 ng/ml. Neither IL-1 nor ceramide induced apoptosis in IEC, but they increased bcl-2 levels and decreased bax and p21 levels without affecting bcl-x and p53 levels. They also caused a slight but significant increase in the G2/M phase. These data suggest a role for ceramide in IBD and suggest a possible mechanism for the enhanced tumorigenic activity in IBD patients.