Altered visceral and psychological stress signal processing in visceral hyperalgesia: Role of central pain processing and local inflammation in the gut.

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The pathophysiology of functional gastrointestinal disorders remains unknown. However, recent data support the role of inflammatory processes in the pathogenesis of irritable bowel syndrome (IBS) and visceral hyperalgesia. Based on our recent data on neuroendocrine-immune interactions in chronic inflammatory diseases, we will test the hypothesis of distrubed functioning of neuroendocrine receptors in the gut, the immune system and the neuroendocrine system of the basis of alterations in the G protein receptor kineases and ß-arrestin machinery. In IBS patients as well as in parallel in a murine model of post-inflammatory visceral hyperalgesia we will analyze the receptor regulation for neuroendocrine and immune responses to visceral and psychological stress, and focus on the gut and afferent signal processing pathways. Theses results will allow new insights into the etiology of functional gastrointestinal disorders and provide a basis for the development of novel therapeutic options via modulation of the nervous system - immune system communication.