IL-1 stimulates ceramide accumulation without inducing apoptosis in intestinal epithelial cells

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 in...

وصف كامل

محفوظ في:
التفاصيل البيبلوغرافية
المؤلف الرئيسي: Homaidan, Fadia R. (author)
مؤلفون آخرون: El-Sabban, Marwan E. (author), Chakroun, Iman (author), El-Sibai, Mirvat (author), Dbaibo, Ghassan S. (author)
التنسيق: article
منشور في: 2002
الوصول للمادة أونلاين:http://hdl.handle.net/10725/2820
http://dx.doi.org/10.1080/09629350210313
http://www.hindawi.com/journals/mi/2002/467015/abs/
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الوصف
الملخص: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.