The regulatory mechanism of sympathetic nerves on eosinophil-associated micr o-inflammation in animals with IBS

本研究旨在探讨交感神经系统(SNS)与微炎症的关系及其可能的机制。在这一年，我建立了母体分离(MS)模型来模拟IBS。该模型表现出对大肠扩张的内脏超敏反应，这是IBS的主要病理生理机制。我用流式细胞术和免疫组织化学方法证实，成年后的MS大鼠结肠内存在微炎症。此外，我还研究了SNS的活跃度。酶联免疫吸附试验结果显示，MS大鼠血清中NE浓度较对照组升高。MS模型组大鼠神经活性标志物高于对照组。综上所述，我证实了MS大鼠表现出SNS的过度激活。此外，我还应用6-OHDA对SNS进行了退行性处理，药理数据表明SNS在结肠免疫细胞的改变中发挥了作用。我还开始建立基因调控方法，专门调节SNS的活动。

This research aims to investigate the relationship and potential mechanism between sympathetic nervous system (SNS) and micro-inflammation. In this year, I established the maternal separation (MS) model to mimic IBS. This model showed visceral hypersensitivity to colorectal distention, which is the main pathophysiology of IBS. I confirmed that there is micro-inflammation in colon of MS rats at adulthood by flowcytometry method and IHC. Besides, I researched the SNS activity. The ELISA result showed that NE concentration in serum increased in the MS rats compared with control. Neural activation markers are higher in MS model rats compared with control. Taken together, I confirmed that MS rats showed over activation of SNS. In addition, I applied the 6-OHDA to degenerate the SNS, the pharmacological data suggested that SNS played a role in immune cell alteration in colon. I also started to establish the genetic modulation approach to specifically modulation SNS activity.