Rutsch Andrina, Kantsjö Johan B, Ronchi Francesca
Maurice Müller Laboratories, Department of Biomedical Research, Universitätsklinik für Viszerale Chirurgie und Medizin Inselspital, University of Berne, Berne, Switzerland.
Front Immunol. 2020 Dec 10;11:604179. doi: 10.3389/fimmu.2020.604179. eCollection 2020.
The human microbiota has a fundamental role in host physiology and pathology. Gut microbial alteration, also known as dysbiosis, is a condition associated not only with gastrointestinal disorders but also with diseases affecting other distal organs. Recently it became evident that the intestinal bacteria can affect the central nervous system (CNS) physiology and inflammation. The nervous system and the gastrointestinal tract are communicating through a bidirectional network of signaling pathways called the gut-brain axis, which consists of multiple connections, including the vagus nerve, the immune system, and bacterial metabolites and products. During dysbiosis, these pathways are dysregulated and associated with altered permeability of the blood-brain barrier (BBB) and neuroinflammation. However, numerous mechanisms behind the impact of the gut microbiota in neuro-development and -pathogenesis remain poorly understood. There are several immune pathways involved in CNS homeostasis and inflammation. Among those, the inflammasome pathway has been linked to neuroinflammatory conditions such as multiple sclerosis, Alzheimer's and Parkinson's diseases, but also anxiety and depressive-like disorders. The inflammasome complex assembles upon cell activation due to exposure to microbes, danger signals, or stress and lead to the production of pro-inflammatory cytokines (interleukin-1β and interleukin-18) and to pyroptosis. Evidences suggest that there is a reciprocal influence of microbiota and inflammasome activation in the brain. However, how this influence is precisely working is yet to be discovered. Herein, we discuss the status of the knowledge and the open questions in the field focusing on the function of intestinal microbial metabolites or products on CNS cells during healthy and inflammatory conditions, such as multiple sclerosis, Alzheimer's and Parkinson's diseases, and also neuropsychiatric disorders. In particular, we focus on the innate inflammasome pathway as immune mechanism that can be involved in several of these conditions, upon exposure to certain microbes.
人类微生物群在宿主生理和病理过程中发挥着重要作用。肠道微生物群的改变,也称为生态失调,不仅与胃肠道疾病有关,还与影响其他远端器官的疾病有关。最近,有证据表明肠道细菌会影响中枢神经系统(CNS)的生理功能和炎症反应。神经系统和胃肠道通过一个双向信号通路网络进行交流,这个网络被称为肠-脑轴,它由多种连接组成,包括迷走神经、免疫系统以及细菌代谢产物和产物。在生态失调期间,这些通路会失调,并与血脑屏障(BBB)通透性改变和神经炎症相关。然而,肠道微生物群在神经发育和发病机制中的作用背后的众多机制仍知之甚少。有几种免疫通路参与中枢神经系统的稳态和炎症反应。其中,炎性小体通路与多种神经炎症性疾病有关,如多发性硬化症、阿尔茨海默病和帕金森病,也与焦虑和抑郁样障碍有关。炎性小体复合物在细胞因接触微生物、危险信号或应激而激活时组装,导致促炎细胞因子(白细胞介素-1β和白细胞介素-18)的产生以及细胞焦亡。有证据表明,微生物群与大脑中炎性小体激活之间存在相互影响。然而,这种影响的确切作用机制尚待发现。在此,我们讨论该领域的知识现状和悬而未决的问题,重点关注在健康和炎症状态下,如多发性硬化症、阿尔茨海默病和帕金森病以及神经精神疾病中,肠道微生物代谢产物或产物对中枢神经系统细胞的作用。特别是,我们关注先天炎性小体通路,它作为一种免疫机制,在接触某些微生物时可能参与其中的几种情况。