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In Vitro and In Vivo Approaches to Determine Intestinal Epithelial Cell Permeability
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Published on: October 19, 2018

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

Fadia R Homaidan1, Marwan E El-Sabban, Iman Chakroun

  • 1Department of Physiology, Faculty of Medicine, American University of Beirut, Lebanon. fh01@aub.edu.lb

Mediators of Inflammation
|April 3, 2002
PubMed

Insights

Interleukin-1 (IL-1) increases ceramide in inflammatory bowel disease (IBD) cells, but does not cause cell death. This suggests ceramide may contribute to increased tumor risk in IBD patients.

Area of Science:

  • Gastroenterology
  • Cell Biology
  • Molecular Biology

Background:

  • Elevated cytokine levels, including interleukin-1 (IL-1), are characteristic of inflammatory bowel disease (IBD).
  • Previous research demonstrated IL-1 activates phospholipid signaling pathways in intestinal epithelial cells (IEC), leading to increased ceramide levels.

Purpose of the Study:

  • To investigate whether ceramide induces apoptosis in intestinal epithelial cells (IEC).

Main Methods:

  • Apoptosis was assessed using annexin-V binding and Hoechst nuclear staining.
  • Western blotting was employed to quantify levels of apoptosis-related proteins (bcl-2, bcl-x, bax, p53, p21).
  • Cell cycle analysis was performed using flow cytometry.

Main Results:

  • Interleukin-1 (IL-1) induced a time- and concentration-dependent increase in ceramide accumulation in IEC.
  • Neither IL-1 nor ceramide treatment resulted in apoptosis of IEC.
  • IL-1 and ceramide modulated apoptosis-related protein expression, increasing bcl-2 and decreasing bax and p21, while bcl-x and p53 remained unchanged.
  • A slight but significant increase in the G2/M phase of the cell cycle was observed.

Conclusions:

  • Ceramide accumulation, induced by IL-1 in IEC, does not directly trigger apoptosis.
  • The observed changes in apoptosis-related proteins and cell cycle suggest a potential role for ceramide in the enhanced tumorigenic activity observed in IBD patients.
Abstract

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