微生物失生症相关的NMDAR高功能在后感染性刺激性肠综合征与内脏过敏症
Lijun Du1, Fangli Cheng2, Weida Shen3
1Department of Gastroenterology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, P. R. China.
Gastroenterology report
|November 26, 2025
概括
肠道微生物失调症可能会在后感染性刺激性肠综合征 (PI-IBS) 的小鼠中触发N-甲基-D-酸盐受体 (NMDAR) 功能过高. 共同住房和抗生素等治疗减少了NMDAR活性和内脏过敏.
科学领域:
- 神经科学是一个神经科学.
- 微生物学 微生物学
- 胃肠病学 胃肠病学
背景情况:
- 刺激性肠综合征 (IBS) 的病理生理学仍然不清楚,其中涉及肠-大脑轴调节失调.
- 后感染性IBS (PI-IBS) 是一种以内脏过敏为特征的亚型.
- 肠道微生物群与PI-IBS中中央N-甲基-D-酸盐受体 (NMDAR) 功能之间的联系正在调查中.
研究的目的:
- 在PI-IBS.小鼠模型中调查肠道微生物失调症和NMDAR高功能之间的关联.
- 探索肠-大脑轴在PI-IBS与内脏过敏症中的作用.
主要方法:
- 使用*Trichinella spiralis*感染建立了一个PI-IBS小鼠模型.
- 视觉敏感性通过腹部撤退反射进行评估.
- 大脑NMDAR活动,c-FOS表达和NMDAR介导电流 (eEPSC) 在胰岛,海马和下丘脑中进行了测量.
主要成果:
- PI-IBS小鼠表现出内脏过敏和在胰岛和海马体中增加c-FOS表达.
- 在PI-IBS小鼠的胰岛和海马体中观察到增强的NMDAR介导的eEPSC.
- 同居和抗生素治疗改善了内脏过敏和减少了NMDAR活性.
结论:
- 肠道微生物群失调是PI-IBS中NMDAR高功能的潜在发起者.
- 向肠道微生物群可能为PI-IBS与内脏过敏症提供治疗策略.
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