The transient receptor potential vanilloid type-1 (TRPV1) is expressed throughout the gastrointestinal tract in myenteric ganglia, muscular layers, and mucosa and TRPV1 expression has been reported on mast cells. (21) TRPV1 is expressed by intestinal sensory nerves and activated by capsaicin, heat, acid, and inflammation. (21) TRPV1 receptor has been implicated as a mechanosensor involved in integrating painful stimuli and in the generation of neurogenic inflammation and hyperalgesia. (22) In rodent models of inflammation, TPRV1 is upregulated with subsequent visceral hyperalgesia to mechanical and chemical stimuli which can be attenuated by TRPV1 antagonism. (22,23) In the rat model, it appears that mast cells are required for upregulation TRPV1 under both infectious and stress conditions. (24) In humans with IBS, there is a significant increase in rectosigmoid TRPV1-immunoreactive fibers and TRPV1 and mast cells are related to abdominal pain scores. (21) Likewise, IBS in quiescent inflammatory bowel disease is associated with an increase in rectosigmoid colon TRPV1-immunoreactive fibers as compared to asymptomatic quiescent IBD or healthy controls and again these fibers correlate with the abdominal pain score. (25) There is evidence of a significant role for TRPV1 in visceral sensitivity and TRPV1 appears to interact with inflammation in general, mast cells in particular, and to be influenced by intestinal infection and stress.