TRPV1 Channel in Pathogenesis of Inflammatory Bowel Disease

Abstract

Abstract—Inflammatory Bowel Disease (IBD) including Ulcerative colitis (UC) and Crohn’s disease (CD) is a group of chronic immune-mediated diseases of the gastrointestinal tract (GIT) with complex pathophysiology and pathogenesis. Although the exact pathophysiological mechanisms are poorly understood, in recent years, studies have described the activation and alteration of nociceptor functions and their signaling pathways in the inflammation development in IBD and associated hyperalgesia, in particular, the key role of the transient receptor potential vanilloid channel 1 (TRPV1) has been demonstrated. The highest expression level of TRPV1 is specific for sensory neurons, however, it can also be expressed by other cell types, including epithelial cells of the intestine and bladder, immunoreactive cells such as lymphocytes, mast and dendritic cells, vascular endothelial cells, etc. An increasing number of studies in various experimental models, including humans, demonstrate that activation of the TRP superfamily channels, which includes TRPV1, can significantly enhance visceral hypersensitivity, mediate the development of inflammation and pain. In this review, we highlight the present knowledge on the structure, functions and potential role of TRPV1 in the pathogenesis of IBD. Much attention is paid to the discussion of the signaling pathways underlying TRPV1 modulation. We propose that further research in this area will contribute to a better understanding of the general mechanisms of inflammatory and pain response formation and may facilitate the development of new therapeutic targets for the treatment of IBD.