Gut Microbiota and the Neuroendocrine System.

Gut Microbiota and the Neuroendocrine System.
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DOI:
10.1007/s13311-017-0600-5
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发表时间:
2018-01
期刊:
Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
影响因子:
--
通讯作者:
Holzer P
Holzer P
中科院分区:
其他
文献类型:
--
作者:
Farzi A;Fröhlich EE;Holzer P

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栖息在所有哺乳动物胃肠道中的微生物生态系统-肠道微生物群-已经与其宿主保持了数千年的共生关系。由于现代技术,由肠道微生物群控制或调节的无数功能开始展现。正在出现的与肠道微生物群密切相互作用的系统之一是身体的主要神经内分泌系统,该系统控制各种身体过程以响应压力,下丘脑-垂体-肾上腺(HPA)轴。这种相互作用至关重要;因为微生物-肠-脑轴的各种疾病与HPA轴的失调有关。本贡献描述了肠道微生物群和HPA轴之间的双向通信,并描绘了潜在的潜在机制。在这方面,重要的是要注意肠道微生物群和HPA轴之间的通信与其他系统密切相关,如免疫系统,肠屏障和血脑屏障,微生物代谢物和肠道激素,以及感觉和自主神经系统。这些通信途径将通过早期生活压力的临床前模型,益生菌和益生元的有益作用,无菌小鼠的证据以及肠道微生物群的益生菌诱导的调节来举例说明。本文的在线版本(10.1007/s13311-017-0600-5)包含补充材料,可供授权用户使用。
The microbial ecosystem that inhabits the gastrointestinal tract of all mammals—the gut microbiota—has been in a symbiotic relationship with its hosts over many millennia. Thanks to modern technology, the myriad of functions that are controlled or modulated by the gut microbiota are beginning to unfold. One of the systems that is emerging to closely interact with the gut microbiota is the body’s major neuroendocrine system that controls various body processes in response to stress, the hypothalamic–pituitary–adrenal (HPA) axis. This interaction is of pivotal importance; as various disorders of the microbiota–gut–brain axis are associated with dysregulation of the HPA axis. The present contribution describes the bidirectional communication between the gut microbiota and the HPA axis and delineates the potential underlying mechanisms. In this regard, it is important to note that the communication between the gut microbiota and the HPA axis is closely interrelated with other systems, such as the immune system, the intestinal barrier and blood–brain barrier, microbial metabolites, and gut hormones, as well as the sensory and autonomic nervous systems. These communication pathways will be exemplified through preclinical models of early life stress, beneficial roles of probiotics and prebiotics, evidence from germ-free mice, and antibiotic-induced modulation of the gut microbiota. The online version of this article (10.1007/s13311-017-0600-5) contains supplementary material, which is available to authorized users.
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