Abstract

development, events that increase intestinal permeability, allowing, consequently, the access of luminal antigens to the mucosa. Food components, microorganisms, and toxins can stimulate local responses by activating immune cells and/or directly sensitizing nerve endings. Primary afferent sensitization could affect responsiveness to visceral stimuli and modify neuropeptide release form nerves, consequently leading to neurogenic inflammation. In fact, mast cell proximity to nerves and its correlation with abdominal pain have been identified in IBS patients. Moreover, the presence of higher amount of corticotropin-releasing hormone in mucosal eosinophils in IBS, as compared to healthy controls, in correlation with psychological stress has been identified, enabling local pain signaling and barrier alterations upon eosinophil degranulation. B lymphocytes and plasma cells are also part of the inflammatory infiltrate and display an activated profile in association with major clinical symptoms in IBS. In this presentation Iwill review themain mechanisms associated with pain signaling in IBS with a special focus on stress-induced activation of the mucosal immune system.

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