Effect of Intestinal Microbiota in Regulating Visceral Hypersensitivity of IBS-D Based on Brain-gut Interacting Mechanism

Li HE; Li YANG; Zhi-wei LING; Min CHEN

doi:10.13422/j.cnki.syfjx.20191129

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Effect of Intestinal Microbiota in Regulating Visceral Hypersensitivity of IBS-D Based on Brain-gut Interacting Mechanism

Review | 更新时间：2021-02-09

- Effect of Intestinal Microbiota in Regulating Visceral Hypersensitivity of IBS-D Based on Brain-gut Interacting Mechanism
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 25, Issue 11, Pages: 224-229(2019)
- 作者机构：
  
  1.成都中医药大学，成都　 610075；
  2.成都中医药大学　附属医院，成都　 610075
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20191129
  CLC： R22; R242; R2-031; R285.5
- Received：13 September 2018，
  
  Published Online：19 February 2019，
  
  Published：05 June 2019
- 稿件说明：
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Li HE, Li YANG, Zhi-wei LING, et al. Effect of Intestinal Microbiota in Regulating Visceral Hypersensitivity of IBS-D Based on Brain-gut Interacting Mechanism[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(11): 224-229.
DOI：

Li HE, Li YANG, Zhi-wei LING, et al. Effect of Intestinal Microbiota in Regulating Visceral Hypersensitivity of IBS-D Based on Brain-gut Interacting Mechanism[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(11): 224-229. DOI： 10.13422/j.cnki.syfjx.20191129.

摘要

腹泻型肠易激综合征(IBS-D)是一种生物心理社会病，也是一种多因素相互作用引起的慢性功能性肠病。IBS-D的发病与内脏感觉异常、肠道动力学异常、肠黏膜微炎性反应、遗传、饮食不耐受等多种因素有关，其中内脏高敏是IBS-D主要的病理生理机制之一，是一种不明原因出现的肠道对寒冷、不良情绪等刺激因素高度敏感的病理过程，但内脏高敏发生机制尚未完全阐明。IBS-D的发病与脑肠互动功能紊乱密切相关，IBS-D患者由于病情反复常常伴随焦虑、抑郁等精神症状，而长期慢性精神应激易诱发及加重IBS-D内脏高敏状态。脑源性神经营养因子(BDNF)及其高亲和受体络氨酸激酶B(TrkB)是研究脑肠互动神经环路的热点，BDNF于中枢神经系统和胃肠道上大量表达，能促进神经系统的发育，维持成熟神经细胞的正常功能，还能调节胃肠道动力和内脏敏感性，是引起和导致神经疼痛敏感的重要细胞因子。肠道微生物是脑肠互动的关键纽带，人精神异常与肠道微生物环境改变引发的肠道症状密切关联。反复精神刺激(如抑郁、焦虑等)可导致肠道菌群的改变，另一方面，肠道菌群结构的改变与神经系统的发育和大脑的功能密切相关。本文以肠道微生物为切入点，以脑—肠轴为轴线，基于BDNF/TrkB通路，探讨肠道菌群调节IBS-D内脏高敏机制的相关性研究。

Abstract

Diarrhea-predominant irritable bowel syndrome (IBS-D) is not only a biological mental disorder

but also a kind of chronic functional bowel disease induced by many factors. The pathogenesis of IBS-D is related to visceral sensory abnormalities

intestinal dynamics abnormalities

intestinal mucosal micro-inflammatory reactions

heredity

dietary intolerance and other factors. The visceral hypersensitivity is one of the main pathophysiology

and refers to an unknown cause of intestinal hypersensitivity to cold

bad mood and other stimuli. However

its mechanism remains unclear. The pathogenesis of IBS-D is closely related to the disturbance of brain and intestinal interaction. IBS-D patients often suffer from anxiety

depression and other psychiatric symptoms due to repeated illness

but long-term chronic mental stress can induce and aggravate IBS-D visceral hypersensitivity. Brain-derived neurotrophic factor (BDNF) and its high-affinity receptor tyrosine kinase B (TrkB) are hotspots in studies about brain-gut axis. BDNF is a highly expressed cytokine in the central nervous system and gastrointestinal tract

and can promote the development of the nervous system

maintain the normal function of mature nerve cells and regulate the gastrointestinal motility and visceral sensitivity. Intestinal microbiota is the key link of brain-gut interaction. Mental disorders are closely related to intestinal symptoms caused by changes in intestinal microbial environment. Repeated mental stimulation can lead to changes in intestinal flora; on the other hand

changes in intestinal flora structure are closely related to the development of the nervous system and the function of the brain. With intestinal microbiota as the study object

this article mainly discusses the effect of intestinal microbiota in regulating visceral hypersensitivity of IBS-D based on brain-gut axis (BDNF/TrkB signaling pathway).

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