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

功能性胃肠道疾病的病理生理学机制尚不清楚。然而，最近的数据支持炎症过程在肠易激综合征(IBS)和内脏痛觉过敏的发病机制中所起的作用。根据我们在慢性炎症性疾病中神经内分泌-免疫相互作用的最新数据，我们将基于G蛋白受体动学和β-arrestin机制的改变来检验神经内分泌受体在肠道、免疫系统和神经内分泌系统中功能紊乱的假说。在IBS患者以及炎症后内脏痛觉过敏的小鼠模型中，我们将分析内脏和心理应激对神经内分泌和免疫反应的受体调节，并重点关注肠道和传入信号处理途径。这些结果将为功能性胃肠道疾病的病因提供新的见解，并为通过调节神经系统-免疫系统通讯来开发新的治疗方案提供基础。

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.