doi: 10.3389/fphar.2014.00072 Inhibition of visceral nociceptors

Abdominal pain is one of the most fre-quent reasons for consulting a doctor. Despite it being a common clinical presen-tation, abdominal pain remains a difficult entity to treat. This is a result of multiple factors including time course (i.e., acute vs. chronic), etiology (e.g., inflammatory vs. post-inflammatory), and stimulus (i.e., mechanical vs. chemical). About 10 % of the population suffer from chronic vis-ceral pain in the form of irritable bowel syndrome (IBS), many of which go undi-agnosed. They are hypersensitive to con-traction and distension of the gut (Barbara et al., 2011; Keszthelyi et al., 2012), but the pathophysiology of pain is poorly under-stood. While the intestinal epithelium is a site of high metabolic activity, includ-ing digestion/absorption, secretion, hor-mone release, and immune interactions, it is generally not viewed as a site of pain modulation. However, there are numer-ous factors at the level of the epithelium capable of modulating pain. This article will highlight the potential role of these factors in nociceptive signaling to identify new therapeutic targets