PDF(Pubmed)
Abstract：
UNASSIGNED: Research is beginning to elucidate the sophisticated mechanisms underlying the microbiota-gut-brain-immune interface, moving from primarily animal models to human studies. Findings support the dynamic relationships between the gut microbiota as an ecosystem (microbiome) within an ecosystem (host) and its intersection with the host immune and nervous systems. Adding this to the effects on epigenetic regulation of gene expression further complicates and strengthens the response. At the heart is inflammation, which manifests in a variety of pathologies including neurodegenerative diseases such as Alzheimer\'s disease, Parkinson\'s disease, and Multiple Sclerosis (MS).
UNASSIGNED: Generally, the research to date is limited and has focused on bacteria, likely due to the simplicity and cost-effectiveness of 16s rRNA sequencing, despite its lower resolution and inability to determine functional ability/alterations. However, this omits all other microbiota including fungi, viruses, and phages, which are emerging as key members of the human microbiome. Much of the research has been done in pre-clinical models and/or in small human studies in more developed parts of the world. The relationships observed are promising but cannot be considered reliable or generalizable at this time. Specifically, causal relationships cannot be determined currently. More research has been done in Alzheimer\'s disease, followed by Parkinson\'s disease, and then little in MS. The data for MS is encouraging despite this.
UNASSIGNED: While the research is still nascent, the microbiota-gut-brain-immune interface may be a missing link, which has hampered our progress on understanding, let alone preventing, managing, or putting into remission neurodegenerative diseases. Relationships must first be established in humans, as animal models have been shown to poorly translate to complex human physiology and environments, especially when investigating the human gut microbiome and its relationships where animal models are often overly simplistic. Only then can robust research be conducted in humans and using mechanistic model systems.
UNASSIGNED: Generally, the research to date is limited and has focused on bacteria, likely due to the simplicity and cost-effectiveness of 16s rRNA sequencing, despite its lower resolution and inability to determine functional ability/alterations. However, this omits all other microbiota including fungi, viruses, and phages, which are emerging as key members of the human microbiome. Much of the research has been done in pre-clinical models and/or in small human studies in more developed parts of the world. The relationships observed are promising but cannot be considered reliable or generalizable at this time. Specifically, causal relationships cannot be determined currently. More research has been done in Alzheimer\'s disease, followed by Parkinson\'s disease, and then little in MS. The data for MS is encouraging despite this.
UNASSIGNED: While the research is still nascent, the microbiota-gut-brain-immune interface may be a missing link, which has hampered our progress on understanding, let alone preventing, managing, or putting into remission neurodegenerative diseases. Relationships must first be established in humans, as animal models have been shown to poorly translate to complex human physiology and environments, especially when investigating the human gut microbiome and its relationships where animal models are often overly simplistic. Only then can robust research be conducted in humans and using mechanistic model systems.
摘要：
■研究开始阐明微生物群-肠道-大脑-免疫界面的复杂机制，从主要的动物模型转向人类研究。研究结果支持作为生态系统（宿主）内的生态系统（微生物组）的肠道微生物群与其与宿主免疫和神经系统的交集之间的动态关系。将其添加到对基因表达的表观遗传调控的影响中,进一步使反应复杂化并增强。心脏是炎症，这表现在各种病理，包括神经退行性疾病，如阿尔茨海默病，帕金森病,和多发性硬化症（MS）。
■一般来说，迄今为止的研究是有限的，集中在细菌上，可能是由于16srRNA测序的简单性和成本效益，尽管分辨率较低，无法确定功能能力/改变。然而,这省略了所有其他微生物群，包括真菌，病毒,和噬菌体，它们正在成为人类微生物组的关键成员。许多研究已经在临床前模型和/或世界上较发达地区的小型人体研究中进行。观察到的关系是有希望的，但目前不能被认为是可靠的或可概括的。具体来说,因果关系目前无法确定。在阿尔茨海默病方面已经做了更多的研究，其次是帕金森病,然后在女士中很少尽管如此，MS的数据令人鼓舞。
■虽然研究仍处于起步阶段，微生物群-肠道-大脑-免疫界面可能是一个缺失的环节，这阻碍了我们在理解上的进步，更不用说预防了，管理,或者缓解神经退行性疾病。关系必须首先在人类中建立，因为动物模型已经被证明很难转化为复杂的人类生理和环境，尤其是在研究人类肠道微生物组及其关系时，动物模型往往过于简单。只有这样，才能在人类中并使用机械模型系统进行强大的研究。
■一般来说，迄今为止的研究是有限的，集中在细菌上，可能是由于16srRNA测序的简单性和成本效益，尽管分辨率较低，无法确定功能能力/改变。然而,这省略了所有其他微生物群，包括真菌，病毒,和噬菌体，它们正在成为人类微生物组的关键成员。许多研究已经在临床前模型和/或世界上较发达地区的小型人体研究中进行。观察到的关系是有希望的，但目前不能被认为是可靠的或可概括的。具体来说,因果关系目前无法确定。在阿尔茨海默病方面已经做了更多的研究，其次是帕金森病,然后在女士中很少尽管如此，MS的数据令人鼓舞。
■虽然研究仍处于起步阶段，微生物群-肠道-大脑-免疫界面可能是一个缺失的环节，这阻碍了我们在理解上的进步，更不用说预防了，管理,或者缓解神经退行性疾病。关系必须首先在人类中建立，因为动物模型已经被证明很难转化为复杂的人类生理和环境，尤其是在研究人类肠道微生物组及其关系时，动物模型往往过于简单。只有这样，才能在人类中并使用机械模型系统进行强大的研究。
