Analysis of epithelial cell shedding and gaps in the intestinal epithelium

Carrie A Duckworth, Alastair J Watson

Research output: Contribution to journalArticlepeer-review

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Abstract

The intestinal barrier is formed by a monolayer of columnar epithelial cells. This barrier is effectively maintained despite the high turnover of epithelial cells in the gut. Defects in the mechanism by which barrier function is maintained are believed to play a central role in the pathogenesis of inflammatory bowel disease (IBD). Proinflammatory cytokines such as TNF-α and IFN-γ are often elevated in inflamed tissue of patients with IBD. In fact, anti-TNF-α therapy is routinely administered to patients with Crohn's disease. We have previously demonstrated that intestinal epithelial cells are shed from the intestine leaving a 'gap' in the epithelium that is able to maintain barrier function. The rate of cell shedding and barrier permeability is substantially increased by the administration of TNF-α. Loss of barrier function at the site of a gap may provide a site of entry for disease-causing bacteria.
Original languageEnglish
Pages (from-to)105-114
Number of pages10
JournalMethods in Molecular Biology
Volume763
DOIs
Publication statusPublished - 2011

Keywords

  • Acriflavine
  • Animals
  • Crohn Disease
  • Cyclic AMP
  • Dextrans
  • Female
  • Fluorescein
  • Fluorescent Dyes
  • Goblet Cells
  • Humans
  • Interferon-gamma
  • Intestine, Small
  • Isoquinolines
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Microscopy, Confocal
  • Permeability
  • Tumor Necrosis Factor-alpha

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