Role of the intestinal barrier in inflammatory bowel disease

摘要

In general, inflammatory processes in the intestine including chronic inflammatory bowel disease (IBD) are accompanied by altered barrier function. This has two main consequences. First, small solutes and water can flow into the lumen and cause leak flux diarrhoea. The second consequence regards larger molecules such as antigens, which under normal conditions cross the epithelial barrier only in small amounts, which allows for immune tolerance induction. However, if the intestinal barrier is impaired, uptake of increased amounts of antigens may aggravate or even initiate inflammation. Besides altered tight junctions, other structural changes in the epithelium such as epithelial cell apoptosis, erosion/ulcer type lesions and transcytosis can also play a role and should be considered. In some regions along the gastrointestinal tract M cells, the follicle-associated epithelium (FAE) above Peyer's patches and transepithelial extrusions of antigen-presenting cells (APC) can contribute to the transport of antigens through the epithelial barrier. This chapter gives an overview of: (a) changes observed in barrier properties in IBD, (b) regulation of intestinal barrier function during inflammation and (c) antibody therapy targeting epithelial dysfunction in IBD.