神经系统与肠道菌群双向调控的研究进展

脑肠-轴是神经系统与肠道菌群之间由神经、内分泌介导的双向调控系统,将大脑和胃肠道之间紧密相连。一方面,肠道菌群可以通过脑肠-轴对神经系统的发育产生影响;另一方面,神经系统也可以通过脑肠-轴改变肠道菌群的结构组成和生物学特征。本文就脑肠轴双向调控的相关研究作一概述,为今后的发展提供理论支持。     

肠道菌群与孤独症谱系障碍的研究进展

孤独症谱系障碍(ASD)是一种主要症状为社会交往障碍、重复刻板行为及狭隘兴趣为特征的神经发育障碍性疾病。病因极为复杂,目前集中在遗传及环境因素两大方面。由于发病机制不明,尚无有效的治疗方法。随着对ASD研究的深入,发现ASD患儿普遍存在胃肠道疾病及肠道菌群的改变。最近的研究显示,肠道神经系统和中枢神经系统之间存在双向互动,称之为微生物-肠-脑轴。肠道菌群通过神经内分泌、神经免疫和肠道神经系统调控大脑功能,进而影响大脑发育和行为。故肠道菌群的失衡可能与ASD的发生有关。本文将总结至今肠道菌群对ASD的作用和相关治疗进展。     

肠道菌群与儿童神经系统发育关系的研究进展

目的 了解肠道菌群对儿童神经系统发育的影响作用。方法 通过“肠道菌群”、“神经系统”、“神经系统疾病”等关键词或主题，在中国知网（CNKI）、 万方、PubMed数据库检索相关文献，经过筛选获取国内外相关文献39篇，以近五年的文献为主，对选取的文献进行整理并撰写综述。结果 儿童时期的肠道菌群存在功能及构成的特点，这一时期肠道菌群可影响大脑小胶质细胞及神经的形成、发育，并且与儿童ADHD、ASD存在关联。结论 肠道菌群参与儿童神经系统的发育，对于维持儿童神经系统的正常功能具有重要意义，同时肠道菌群可能通过多方面作用参与神经系统疾病的发生、发展。     

儿童孤独症谱系障碍与肠道菌群家族的那些事

<正>孤独症谱系障碍是一种严重影响儿童成长的神经发育障碍,典型的临床表现为语言沟通障碍、社交障碍、兴趣狭窄及行为重复刻板。男童发病率明显高于女童。近年来,很多研究发现肠道中的菌群家族在大脑发育中发挥着非常重要的作用,菌群家族与大脑之间通过微生物—肠—脑轴进行信息互通交流,对大脑发育及其功能产生影响。很大部分孤独症谱系障碍患儿存在消化道不适症状,如腹痛、腹泻、恶心、腹胀、便秘等,     

肠道菌群对神经退行性疾病影响的研究进展

神经退行性疾病严重影响老年生存质量。其病因尚不明确且没有有效的治疗手段。研究表明,胃肠道通过肠脑轴与中枢神经系统进行交流,肠道菌群失调往往引发为神经系统症状,说明神经性退行性疾病的发病受到肠道菌群的影响。我们通过肠道菌群对神经退行性疾病的影响的研究进展进行综述,为研究神经性退行性疾病的机制及其有效防治提供新视角。     

肠道微生态与抑郁症的相关性及预防治疗展望

<正>肠道菌群与人体相互作用及影响的统一体称为肠道微生态(gut microflora),是人体最大的微生态系统,与人类的健康和疾病密切相关。过去十年已经有大量研究及证据表明,肠道微生态可调节大脑功能。随着"脑-肠-菌群"轴学说的提出和证实,微生态的相关研究已涉及中枢神经系统疾病,其中包括与抑郁相关的行为。抑郁症患病率高、疾病负担重,且发病率呈逐年上升趋势,严重危害公众的身心健康及生命~([1]),如何将     

注意缺陷多动障碍与肠道菌群的关系研究进展

注意缺陷多动障碍(ADHD)是儿童最常见的神经发育障碍之一,表现为与发育程度不相符的注意力不集中、多动、冲动,并伴有社交、学业等方面的功能损害。目前ADHD的病因尚不清楚,普遍认为ADHD是由遗传、环境及其交互作用共同引起的一种行为疾病,可能与额叶纹状体脑功能障碍和单胺神经递质系统功能受损有关。不同的肠道菌群可产生不同的神经递质,通过微生物-肠-脑轴的双向交流参与对中枢神经系统的调控。因此,了解肠道菌群、微生物-肠-脑轴和ADHD之间的相互作用可能为ADHD的早期干预和治疗开辟新的途径。     

微生物–肠–脑轴：环境污染物致毒新靶点

有机污染物、抗生素、重金属、农药等环境污染物的暴露和摄食已知能导致多种形式的神经系统疾病，但其中确切机制尚未完全阐明。肠–脑轴是一个连接肠道和大脑的重要且复杂的路径网络。肠道微生物作为肠道和大脑沟通桥梁搭建的首要介质，对环境中的各类污染物十分敏感。其可作为环境污染物神经毒性的作用靶点以调节免疫应答、物质代谢或直接影响神经元和神经信号的传导进而调控污染物对大脑炎性反应、神经递质分泌、内源性抗氧化防御系统功能、血脑屏障完整性和线粒体功能等的干扰过程。本文就肠–脑互作机制，以及环境污染物通过微生物–肠–脑轴介导宿主神经系统发育和功能的研究结果做简要综述，望为未来环境污染物、肠道微生物和人类健康之间深层关系提供前瞻性见解，并为寻找相关神经疾病的防治方法的提供参考。     

肠道微生物与儿童孤独症谱系障碍的研究进展

孤独症谱系障碍(ASD)是一种严重的神经系统广泛性发育障碍疾病,其核心症状是社会功能的缺失,社会交流障碍、兴趣范围局限及刻板行为等,由遗传和环境因素相互作用而引起。肠道微生物是存在于肠道中数量众多的微生物,不仅影响消化吸收能力,而且通过肠-脑轴影响大脑的发育和功能。特定的益生菌可以调节人体微生态的平衡,维持正常的代谢吸收和免疫防御功能。婴幼儿发育关键期肠道微生物失调会增加儿童ASD的风险,并通过神经内分泌、免疫、代谢产物途径影响儿童ASD的发展,益生菌治疗有望成为治疗儿童ASD的新型辅助治疗方法     

微生物-肠-脑轴在新生儿缺氧缺血性脑病发病机制中的研究进展

新生儿缺氧缺血性脑病 (HIE) 是新生儿期有较高致残率和致死率的疾病之一。近年来研究显示,新生儿脑部的缺氧缺血性损伤与微生物-肠-脑轴参与的神经系统氧化应激和组织线粒体功能障碍有关,但其分子机制尚不明确;且HIE最关键的环节是二次能量衰竭的发生,两次能量衰竭之间的“潜伏期”就是所谓的治疗“时间窗”,是减轻脑损伤的神经保护措施能被成功应用的最佳时间。本文综述了“微生物-肠-脑轴”参与氧化应激在HIE发病机制中的研究进展,希望通过该轴作用在HIE治疗“时间窗”内,减轻氧化应激对大脑的损伤,从而为肠道菌群与大脑之间的相互作用增加一个新的维度,为HIE的防治打开一扇门。     

Gut-Brain-Microbiota Axis: Antibiotics and Functional Gastrointestinal Disorders

Gut microbiota composition and function are major areas of research for functional gastrointestinal disorders. There is a connection between gastrointestinal tract and central nervous system and this is mediated by neurotransmitters, inflammatory cytokines, the vagus nerve and the hypothalamic-pituitary-adrenal axis. Functional gastrointestinal disorders are prevalent diseases affecting more than one third of the population. The etiology of these disorders is not clarified. Visceral hyperalgesia is the main hypothesis for explaining clinical symptoms, however gut-brain axis disorder is a new terminology for functional disorders. In this review, microbiota-gut-brain axis connection pathways and related disorders are discussed. Antibiotics are widely used in developed countries and recent evidence indicates antibiotic-induced dysbiosis as an important factor for functional disorders. Antibiotics exert negative effects on gut microbiota composition and functions. Antibiotic-induced dysbiosis is a major factor for occurrence of post-infectious irritable bowel syndrome. Cognitive and mood disorders are also frequent in functional gastrointestinal disorders. Animal and human trials show strong evidence for the causal relationship between gut microbiota and brain functions. Therapeutic implications of these newly defined pathogenic pathways are also discussed.     

The Microbiota–Gut–Brain Axis in Depression: The Potential Pathophysiological Mechanisms and Microbiota Combined Antidepression Effect

Depression is a kind of worldwide mental illness with the highest morbidity and disability rate, which is often accompanied by gastrointestinal symptoms. Experiments have demonstrated that the disorder of the intestinal microbial system structure plays a crucial role in depression. The gut–brain axis manifests a potential linkage between the digestion system and the central nervous system (CNS). Nowadays, it has become an emerging trend to treat diseases by targeting intestinal microorganisms (e.g., probiotics) and combining the gut–brain axis mechanism. Combined with the research, we found that the incidence of depression is closely linked to the gut microbiota. Moreover, the transformation of the gut microbiota system structure is considered to have both positive and negative regulatory effects on the development of depression. This article reviewed the mechanism of bidirectional interaction in the gut–brain axis and existing symptom-relieving measures and antidepression treatments related to the gut microbiome.     

脑-肠轴与多囊卵巢综合征发病关系的研究进展

多囊卵巢综合征（polycystic ovary syndrome，PCOS）是一种常见的复杂内分泌紊乱性疾病，常伴有高雄激素血症、排卵障碍、胰岛素抵抗和肥胖。近年来临床上大量研究发现肥胖与PCOS关系密切，超过60%的PCOS患者表现为超重或肥胖。食欲调控和能量摄入对维持能量平衡和体质量至关重要。脑-肠轴是肠内细菌与大脑间的双向通信系统，胃肠道系统可通过产生脑肠肽参与到脑-肠互动中，主要包括生长激素释放多肽、胰高血糖素样肽-1、酪酪肽和胆囊收缩素。另外，肠道菌群的改变以及其与脑-肠轴之间的相互作用可能参与PCOS的发病。重点阐述脑-肠轴参与PCOS发病的可能机制及探讨与之相关的PCOS新型治疗方法。     

Psychophysiological Effects of Lactobacillus plantarum PS128 in Patients with Major Depressive Disorder: A Preliminary 8-Week Open Trial

Recent studies have suggested that gut–brain axis may be one of the mechanisms of major depression disorder (MDD). The current study aimed to investigate the effects of Lactobacillus plantarum PS128 (PS128) on psychophysiology in patients with MDD. We recruited 11 patients with MDD and gave them PS128 for 8 weeks. We compared depression symptoms, serum markers of inflammation and gut permeability, and gut microbiota before and after 8-week intervention and also explored the correlations among symptoms, biomarkers, and gut microbiota. After 8-week PS128 intervention, scores of Hamilton Depression Rating Scale-17 and Depression and Somatic symptoms Scale significantly decreased. Serum levels of high sensitivity c-reactive protein, interluekin-6, and tumor necrosis factor-α, zonulin and intestinal fatty acid binding protein, and the composition of gut microbiota did not significantly change after 8-week PS128 intervention. However, we found changes of some genera were correlated with changes of symptoms and biomarkers. In conclusion, this is an open trial with small sample size and has several limitations. The results need to be verified by randomized, double-blind, placebo-controlled trial with larger sample size.     

肠道菌群与多囊卵巢综合征代谢异常的研究进展

多囊卵巢综合征(polycystic ovary syndrome,PCOS)患者的高雄激素血症、胰岛素抵抗和肥胖之间相互影响,其代谢异常成为PCOS患者急需解决的问题之一.人体肠道中存在着丰富的微生物,肠道菌群与宿主终生相伴,互利共生,成为肿瘤、免疫性疾病和代谢性疾病的研究热点,近年对PCOS患者肠道菌群及其与代谢异...     

The Immunopathogenesis of Alzheimer’s Disease Is Related to the Composition of Gut Microbiota

The microbiota–gut–brain axis plays an important role in the development of neurodegenerative diseases. Commensal and pathogenic enteric bacteria can influence brain and immune system function by the production of lipopolysaccharides and amyloid. Dysbiosis of the intestinal microbiome induces local and consecutively systemic immune-mediated inflammation. Proinflammatory cytokines then trigger neuroinflammation and finally neurodegeneration. Immune-mediated oxidative stress can lead to a deficiency of vitamins and essential micronutrients. Furthermore, the wrong composition of gut microbiota might impair the intake and metabolization of nutrients. In patients with Alzheimer’s disease (AD) significant alterations of the gut microbiota have been demonstrated. Standard Western diet, infections, decreased physical activity and chronic stress impact the composition and diversity of gut microbiota. A higher abundancy of “pro-inflammatory” gut microbiota goes along with enhanced systemic inflammation and neuroinflammatory processes. Thus, AD beginning in the gut is closely related to the imbalance of gut microbiota. Modulation of gut microbiota by Mediterranean diet, probiotics and curcumin can slow down cognitive decline and alter the gut microbiome significantly. A multi-domain intervention approach addressing underlying causes of AD (inflammation, infections, metabolic alterations like insulin resistance and nutrient deficiency, stress) appears very promising to reduce or even reverse cognitive decline by exerting positive effects on the gut microbiota.     

Medicinal Plants and Their Impact on the Gut Microbiome in Mental Health: A Systematic Review

Background: Various neurocognitive and mental health-related conditions have been associated with the gut microbiome, implicating a microbiome–gut–brain axis (MGBA). The aim of this systematic review was to identify, categorize, and review clinical evidence supporting medicinal plants for the treatment of mental disorders and studies on their interactions with the gut microbiota. Methods: This review included medicinal plants for which clinical studies on depression, sleeping disorders, anxiety, or cognitive dysfunction as well as scientific evidence of interaction with the gut microbiome were available. The studies were reported using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. Results: Eighty-five studies met the inclusion criteria and covered thirty mental health-related medicinal plants with data on interaction with the gut microbiome. Conclusion: Only a few studies have been specifically designed to assess how herbal preparations affect MGBA-related targets or pathways. However, many studies provide hints of a possible interaction with the MGBA, such as an increased abundance of health-beneficial microorganisms, anti-inflammatory effects, or MGBA-related pathway effects by gut microbial metabolites. Data for Panax ginseng, Schisandra chinensis, and Salvia rosmarinus indicate that the interaction of their constituents with the gut microbiota could mediate mental health benefits. Studies specifically assessing the effects on MGBA-related pathways are still required for most medicinal plants.     

Multiple sclerosis and the microbiota: Progress in understanding the contribution of the gut microbiome to disease

Multiple sclerosis (MS), a neurological autoimmune disorder, has recently been linked to neuro-inflammatory influences from the gut. In this review, we address the idea that evolutionary mismatches could affect the pathogenesis of MS via the gut microbiota. The evolution of symbiosis as well as the recent introduction of evolutionary mismatches is considered, and evidence regarding the impact of diet on the MS-associated microbiota is evaluated. Distinctive microbial community compositions associated with the gut microbiota of MS patients are difficult to identify, and substantial study-to-study variation and even larger variations between individual profiles of MS patients are observed. Furthermore, although some dietary changes impact the progression of MS, MS-associated features of microbiota were found to be not necessarily associated with diet per se. In addition, immune function in MS patients potentially drives changes in microbial composition directly, in at least some individuals. Finally, assessment of evolutionary histories of animals with their gut symbionts suggests that the impact of evolutionary mismatch on the microbiota is less concerning than mismatches affecting helminths and protists. These observations suggest that the benefits of an anti-inflammatory diet for patients with MS may not be mediated by the microbiota per se. Furthermore, any alteration of the microbiota found in association with MS may be an effect rather than a cause. This conclusion is consistent with other studies indicating that a loss of complex eukaryotic symbionts, including helminths and protists, is a pivotal evolutionary mismatch that potentiates the increased prevalence of autoimmunity within a population.