Influence of Toll-like receptor 2 and interleukin 10 on the intestinal epithelial barrier and their roles in inflammatory bowel disease

Different polymorphisms in key genes of innate and adaptive immunity disrupt the intestinal host-microbiotic balance in inflammatory bowel disease (IBD). In most cases these alterations affect the maintenance of the intestinal epithelium. Because of this, actions taken in order to reinforce or help intestinal epithelium recovery can provide benefits to idiopathic illnesses such as IBD. With this in mind, several studies support the idea that actions derived from the Toll-like receptor (TLR) 2 of the epithelial cells may help to maintain the epithelial barrier. However, in inflammatory conditions TLR-2 disappears from the intestinal epithelium and acquires a pivotal role in dendritic cells. In this event, the interleukin (IL)-10 production by sub-epithelial dendritic cells mediated by TLR-2 activation, thus leading to T-reg phenotypes in the lamina propria, may favour the recovery from epithelial damage. Therefore, the TLR-2/IL-10 axis can help to reinforce and recover the epithelial lining in IBD. In this way, several data suggest that early epithelial repair diminishes the antigen load reaching the lamina propria, which reduces inflammation and improves therapeutic performance. However, there is currently a lack of knowledge regarding molecular regulation of epithelial barrier by TLR-2 and IL-10.