压力与肠道-大脑轴:炎症视角

IF 3.5 3区 医学 Q2 NEUROSCIENCES
Julia Morys, Andrzej Małecki, Marta Nowacka-Chmielewska
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引用次数: 0

摘要

肠脑轴(GBA)在维持体内平衡方面发挥着主导作用,并有助于维持心理健康。支撑该轴的通路从与神经系统的宏观相互作用扩展到分子信号,包括微生物代谢物、紧密连接蛋白表达或炎症期间释放的细胞因子。GBA 功能失调多次与焦虑和抑郁样行为的发生发展有关。最近有文献强调了GBA改变的炎症方面的重要性。在此,我们总结了目前有关 GBA 信号传导的报道,其中涉及肠道和血脑屏障(BBB)内的免疫反应。我们还强调了应激反应对改变屏障通透性的影响,以及根据最新的动物研究,通过服用益生菌或移植微生物群来恢复微生物群的治疗潜力。对各种应激模型进行的大多数研究表明,焦虑和抑郁样行为、肠道微生物群失调、肠道通透性破坏与 BBB 的完整性同时发生变化之间存在关联。因此可以推测,在压力条件下,BBB 沟通受损可能是肠道微生物群影响大脑功能的一个重要机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Stress and the gut-brain axis: an inflammatory perspective
The gut-brain axis (GBA) plays a dominant role in maintaining homeostasis as well as contributes to mental health maintenance. The pathways that underpin the axis expand from macroscopic interactions with the nervous system, to the molecular signals that include microbial metabolites, tight junction protein expression, or cytokines released during inflammation. The dysfunctional GBA has been repeatedly linked to the occurrence of anxiety- and depressive-like behaviors development. The importance of the inflammatory aspects of the altered GBA has recently been highlighted in the literature. Here we summarize current reports on GBA signaling which involves the immune response within the intestinal and blood-brain barrier (BBB). We also emphasize the effect of stress response on altering barriers' permeability, and the therapeutic potential of microbiota restoration by probiotic administration or microbiota transplantation, based on the latest animal studies. Most research performed on various stress models showed an association between anxiety- and depressive-like behaviors, dysbiosis of gut microbiota, and disruption of intestinal permeability with simultaneous changes in BBB integrity. It could be postulated that under stress conditions impaired communication across BBB may therefore represent a significant mechanism allowing the gut microbiota to affect brain functions.
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来源期刊
CiteScore
5.70
自引率
2.10%
发文量
669
审稿时长
14 weeks
期刊介绍: Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.
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