Role of Toll-like receptors in inflammatory bowel diseases

摘要

The intestinal epithelium constitutes an anatomical as well as immunological barrier that forms a bipolar interface between the diverse populations of lumenal microbes and immune cells of the underlying lamina propria. The intestinal epithelial barrier must exert a highly defined process of discrimination - excluding potential host-threatening agents from microbial species while allowing host-beneficial substances (e.g. nutrients) to permeate. Mucosal imbalance within this complex network of cell and microbial interactions appears to play a key role in the pathogenesis of inflammatory bowel diseases (IBD). To counteract potential harmful effects of lumenal toxins and to protect barrier homeostasis, intestinal epithelial cells (IEQ produce several defensive factors, including trefoil peptides, mucins1 and defensins2. However, these host-protective defence mechanisms are severely dysregulated in colitis.