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

交感神经对IBS动物嗜酸性粒细胞相关微炎症的调节机制

• 批准号: 22K15656
• 负责人: 段 ショウキ
• 金额: $ 2.91万
• 依托单位: Hyogo Medical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Early-Career Scientists
• 财政年份: 2022
• 资助国家: 日本
• 起止时间: 2022-04-01 至 2025-03-31
• 项目状态: 未结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-22K15656/
• 关键词: SNS; IBS; Micro-inflammation; Visceral pain; sympathetic nervous; eosinophil

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.

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机制。在这一年中，我建立了母亲分离（MS）模型来模拟IBS。该模型表现出内脏对结直肠扩张的高敏感性，这是IBS的主要病理生理学。通过流式细胞术和免疫组化证实成年期MS大鼠结肠存在微炎症反应。此外，我研究了SNS活动。ELISA结果显示，MS大鼠血清NE浓度较对照组升高。与对照组相比，MS模型大鼠的神经激活标志物更高。综上所述，我证实了MS大鼠表现出过度激活的SNS。此外，本研究还应用6-OHDA对SNS进行了变性处理，药理学数据表明SNS在结肠免疫细胞改变中发挥作用。 我也开始建立基因调节方法来专门调节SNS活动。