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Related Experiment Videos

Disrupted barrier function through epithelial cell apoptosis.

Joerg-Dieter Schulzke1, Christian Bojarski, Sebastian Zeissig

  • 1Medizinische Klinik I, Department of Gastroenterology, Infectious Diseases and Rheumatology, Charité, Campus Benjamin Franklin, 12200 Berlin, Germany. Joerg.Schulzke@Charite.de

Annals of the New York Academy of Sciences
|October 24, 2006
PubMed
Summary
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Epithelial apoptosis increases intestinal permeability, causing diarrhea and antigen entry. Blocking TNF-alpha with infliximab restores barrier function in Crohn's disease by reducing epithelial apoptosis.

Area of Science:

  • Gastroenterology
  • Cell Biology
  • Immunology

Background:

  • Epithelial barrier integrity is crucial for intestinal health, regulated by tight junctions and apoptosis.
  • Epithelial apoptosis, or programmed cell death, can compromise this barrier.
  • Understanding the role of apoptosis in inflammatory bowel disease (IBD) is vital for developing targeted therapies.

Purpose of the Study:

  • To investigate the functional role of epithelial apoptosis in intestinal barrier function.
  • To examine the impact of pro-inflammatory cytokines on epithelial apoptosis and conductivity.
  • To assess changes in epithelial apoptosis in patients with inflammatory bowel disease.

Main Methods:

  • Utilized cell culture models and patient tissue samples from inflammatory bowel disease (IBD) patients.

Related Experiment Videos

  • Measured epithelial conductance and apoptotic rates.
  • Analyzed the effects of tumor necrosis factor-alpha (TNF-alpha) and interleukin-13 (IL-13).

    • Main Results:

    • Epithelial apoptoses were identified as sites of increased conductance in the intestinal epithelium.
    • Pro-inflammatory cytokines, particularly TNF-alpha, significantly upregulate apoptotic rate and conductivity.
    • Apoptotic rates were elevated in ulcerative colitis and Crohn's disease (CD) tissues compared to controls.
    • Cytokine-induced apoptosis was found to be more functionally significant than spontaneous apoptosis.

    Conclusions:

    • Epithelial apoptosis contributes to leak flux diarrhea and allows antigen translocation, perpetuating inflammation in IBD.
    • TNF-alpha and IL-13 are key inducers of epithelial apoptosis.
    • Therapeutic blockade of TNF-alpha, as with infliximab, can restore intestinal barrier function in CD by reducing epithelial apoptosis.