脑-肠轴有助于应激相关疾病的神经进展。

Modern trends in pharmacopsychiatry Pub Date : 2017-01-01 Epub Date: 2017-07-24 DOI:10.1159/000470813
Kieran Rea, Timothy G Dinan, John F Cryan
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引用次数: 27

摘要

人们越来越重视肠道微生物(人类胃肠道微生物群)的复杂性和多样性与大脑健康之间的关系。微生物-肠-脑轴是一个由组织和器官组成的动态矩阵,包括大脑、腺体、肠道、免疫细胞和胃肠道微生物群,它们以复杂的多向方式交流以维持体内平衡。这种环境的改变可能通过改变生理过程,包括下丘脑-垂体-肾上腺轴激活、神经递质系统、免疫功能和炎症反应,促进应激相关疾病的神经进展。虽然适当的、协调的生理反应,如免疫反应或应激反应,是生存所必需的,但反复或长期暴露于压力下可能使个人更容易处于一种脆弱的状态,使他们更容易患上与压力有关的疾病。在本章中,胃肠道微生物群参与应激和免疫介导的神经内分泌、免疫和神经递质系统的调节以及相应的行为。我们还关注了共生肠道微生物群调节神经炎症的机制,并进一步致力于利用我们对微生物群-肠道-脑轴在神经炎症过程导致的应激相关疾病的神经进展中的作用的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Brain-Gut Axis Contributes to Neuroprogression in Stress-Related Disorders.

There is a growing emphasis on the relationship between the complexity and diversity of the microorganisms that inhabit our gut (human gastrointestinal microbiota) and brain health. The microbiota-gut-brain axis is a dynamic matrix of tissues and organs including the brain, glands, gut, immune cells, and gastrointestinal microbiota that communicate in a complex multidirectional manner to maintain homeostasis. Changes in this environment may contribute to the neuroprogression of stress-related disorders by altering physiological processes including hypothalamic-pituitary-adrenal axis activation, neurotransmitter systems, immune function, and inflammatory responses. While appropriate, coordinated physiological responses, such as immune or stress responses, are necessary for survival, the contribution of repeated or chronic exposure to stress may predispose individuals to a more vulnerable state leaving them more susceptible to stress-related disorders. In this chapter, the involvement of the gastrointestinal microbiota in stress- and immune-mediated modulation of neuroendocrine, immune, and neurotransmitter systems and the consequential behavior is considered. We also focus on the mechanisms by which commensal gut microbiota can regulate neuroinflammation and further aim to exploit our understanding of their role in the effects of the microbiota-gut-brain axis on the neuroprogression of stress-related disorders as a consequence of neuroinflammatory processes.

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