Confocal Laser Endomicroscopy in the Management of IBD: Clearly Superior?

Excerpt

The intestinal epithelium forms a barrier against the entry of toxins, antigens and microbes from the environment. The epithelial cell itself, the tight junctions between the epithelial cells, and the mucus covering the epithelium together with antimicrobial peptides in the mucus all contribute to the barrier function of the epithelium. Abnormalities of these three elements are now well documented to substantially contribute to the pathogenesis of inflammatory bowel disease (IBD). Recently, a fourth component to this barrier has come to light; understanding this component requires review of the cell dynamics of the intestinal epithelium. The intestinal epithelium arises from stem cells located at the base of crypts, which then migrate up the crypt-villus axis in the case of the small intestine or to the surface of the colon from where they are shed. This shedding process could potentially create a gap in the epithelial monolayer thereby compromising the integrity of the epithelial barrier. In health, the integrity of the barrier is maintained during shedding by an overall redistribution of tight junctional proteins around the epithelial cell plugging the gap created by the shedding cell. When the intestine is inflamed, cytokines such as tumor necrosis factor (TNF)-α induced apoptosis in the epithelium, greatly increasing the rate of epithelial shedding. In these circumstances adjacent epithelial cells are shed, creating gaps that are too large to be sealed by a redistribution of tight junction-associated proteins [1]. …