肠道菌群代谢产物在鼠伤寒沙门菌感染中的作用研究进展

人和动物肠道内生存着多种多样的微生物群体,它们与宿主共同进化,对宿主的健康至关重要。肠道菌群可以发酵宿主难以消化的复杂碳水化合物,为宿主肠道细胞提供能量,同时其代谢产物对肠道病原菌沙门菌的感染产生着重要影响。正常情况下,肠道菌群代谢产物如丁酸与丙酸可以抑制沙门菌在肠道中的定植或者毒力基因的表达,而在肠道菌群受到扰乱时,其代谢的琥珀酸盐和1,2 丙二醇等物质却能促进沙门菌增殖。近年来,越来越多的研究揭示了肠道菌群代谢产物对沙门菌感染的影响。本综述通过总结近年来关于鼠伤寒沙门菌入侵时肠道菌群代谢产物改变的研究,综合阐述了肠道菌群代谢产物影响沙门菌感染的机制。     

动物宿主——肠道微生物代谢轴研究进展

肠道中栖息着数量庞大且复杂多样的微生物菌群,在维持宿主肠道微环境稳态中发挥重要作用。微生物菌群可以利用宿主肠道的营养素,发酵产生代谢产物,与宿主机体形成宿主—微生物代谢轴(host-microbe metabolic axis)。该代谢轴既能影响营养素吸收和能量代谢,又可调控宿主各项生理过程。本文主要阐述宿主-肠道微生物代谢轴的概念、肠-肝轴、肠-脑轴、肠道微生物与宿主肠道代谢轴的互作以及对机体健康的影响。     

肠道菌群相关代谢产物影响骨代谢的研究进展

肠道菌群是包括细菌和真菌在内的多种微生物的总称,定植于宿主肠道中,与宿主形成复杂的共生关系,在维持人体健康中起重要作用。目前肠道菌群调节骨代谢已经成为研究的热点,除了肠道菌群影响骨代谢外,肠道菌群的代谢产物也可以影响骨代谢。肠道菌群代谢产物,如短链脂肪酸、色氨酸、胆汁酸、硫化氢和维生素B等都对骨代谢有直接或间接的影响。本文对肠道菌群相关代谢产物影响骨代谢的机制进行探讨,以期为治疗骨质疏松症提供新的思路。

     

肠道稳态与代谢综合征

代谢综合征(metabolic syndrome,MS)是具有多样临床表现的物质代谢紊乱,包括肥胖和胰岛素抵抗等。它能增加糖尿病和心血管的发病率。目前它的病因尚不明确,与环境、免疫、遗传等因素有关。研究表明代谢综合征患者肠道菌群结构较正常人有所改变,肠道稳态被打破。宿主共生菌在正常生理条件下,参与到宿主的物质代谢、营养吸收、免疫反应等过程中,同时其也受宿主基因、营养情况和生活方式的影响。不断深入了解宿主和肠道菌群之间的作用关系,能有效提出具有针对性的治疗代谢综合征的个性化防治策略。     

肠道菌群及其代谢产物与高血压的相关性研究进展

高血压是一种常见的慢性疾病, 是世界上最严重的公共卫生问题之一, 其发病机制尚未完全阐明。人体肠道菌群与疾病的发生相关, 高血压患者或高血压动物模型肠道中均存在菌群失调, 肠道菌群及其代谢产物被证明与高血压的发生密切相关。本文综述了国内外的相关研究进展, 从与高血压相关的肠道菌群种类、代谢产物及作用机制等多方面讨论了肠道菌群及其代谢产物与高血压的相关性, 以期从肠道菌群及其代谢产物的角度对高血压的防治提供思路和方法。

     

从肠道菌群角度认识阿尔茨海默病的潜在发病机制

过去10年中,人们逐渐认识到肠道微生物群的多样性及菌群平衡在维护宿主健康中发挥的作用。肠道微生物及其代谢产物通过一系列的生化、免疫和生理功能环节与宿主进行交流,从而影响宿主的稳态和健康。阿尔茨海默病(Alzheimer’s disease,AD)是一种复杂的神经退行性疾病,其易感性和发展过程受年龄、遗传和表观遗传等因素的影响。研究发现,肠道微生物群的紊乱(组成改变和易位)与神经系统疾病(AD)有关,胃肠道通过肠脑轴与中枢神经系统进行沟通,包括对神经的直接作用、内分泌途径和免疫调控方式。动物模型、粪便菌群移植及益生菌干预为肠道菌群与AD的相关性提供了证据。外漏的细菌代谢产物可能直接损害神经元功能,也可能诱发神经炎症,促进AD的发病。本文主要综述了肠道微生物群与AD的关联和作用机制,以期为通过改善肠道菌群结构预防AD的可能干预措施提供依据。     

肠道微生物调控宿主食欲的研究进展

肠道微生物与宿主代谢相互作用,可调节机体的生理功能。宿主机体中存在"微生物-肠道-大脑轴",肠道菌群可通过多种途径影响中枢神经系统,进而对宿主摄食等行为产生影响。食物中不易被宿主消化吸收的膳食纤维等营养物质,被肠道微生物发酵可产生多种代谢产物,这些代谢产物作为信号分子可通过不同途径介导中枢神经系统,进而调控宿主食欲。本文主要综述了肠道微生物及其代谢产物对中枢神经系统与宿主食欲的影响及其可能的调控途径与机制,以加深肠道微生物在调控宿主食欲方面的新认识。     

microRNA 对宿主和肠道微生物互作的调控

摘要:肠道内环境是宿主和肠道微生物菌群互作的结果,肠道菌群一方面通过抗原物质调节肠道组织的免疫稳定,另一方面,肠道菌群参与糖、脂、蛋白质代谢,产生的代谢产物能够调控细菌营养代谢、群体结构和肠道组织的营养吸收等。microRNA是宿主细胞内调控基因表达的重要因子,肠道微生物菌群不仅调控宿主mRNA的转录,同时也影响某些基因的转录后修饰。研究表明,肠道菌群通过与宿主肠道组织互作,调节肠上皮组织内某些参与炎症应答和屏障功能的microRNA 的表达。本文介绍了肠道微生物与宿主互作的基本内容,对microRNA在肠道微生物与宿主互作和肠道健康中的调节进行综述。     

溃疡性结肠炎肠道菌群及其代谢产物的研究进展

溃疡性结肠炎(UC)是一种病因尚未阐明的慢性非特异性肠道炎症疾病,多认为由易感人群免疫反应紊乱所致,疾病负担重,严重影响生活质量。近年随着人们生活方式的改变与诊断水平的提升,UC发病率和患病率逐年增加。研究显示肠道菌群及其代谢产物在UC的发生发展过程中起着关键作用,包括调节免疫、参与信号转导、保护肠黏膜屏障和营养代谢等,肠道菌群代谢产物的紊乱及微生态的失衡在炎症的形成及发展、免疫应激及稳态等方面产生重要影响。该文对近年来肠道菌群及其代谢产物与UC关系的相关研究作一综述,并探讨基于肠道菌群以及其代谢产物的UC防治策略。     

短链脂肪酸对肠黏膜屏障的影响

肠黏膜屏障具有将致病性抗原等肠内物质与内环境隔离的功能,以维持内环境的相对稳定和机体的正常生命活动。其功能的维持依赖于人肠黏膜上皮细胞、肠道内正常菌群、肠道内分泌物和肠相关免疫细胞之间的功能协调,而其功能的发挥又受体内许多信号分子的影响。短链脂肪酸（short-chain fatty acids,SCFAs）就是其中一种重要的信号分子。SCFAs是肠道菌群的主要代谢产物之一,是肠道菌群与宿主代谢相互作用的媒介。宿主体内的SCFAs主要来自肠道菌群对膳食纤维的酵解,越来越多的研究证实,SCFAs不仅可以被肠道菌群利用,还可调节肠黏膜屏障及多种组织器官的代谢。本文主要就SCFAs对肠黏膜屏障的影响进行综述。

     

Endocrine organs of cardiovascular diseases: Gut microbiota

Gut microbiota (GM) is a collection of bacteria, fungi, archaea, viruses and protozoa, etc. They inhabit human intestines and play an essential role in human health and disease. Close information exchange between the intestinal microbes and the host performs a vital role in digestion, immune defence, nervous system regulation, especially metabolism, maintaining a delicate balance between itself and the human host. Studies have shown that the composition of GM and its metabolites are firmly related to the occurrence of various diseases. More and more researchers have demonstrated that the intestinal microbiota is a virtual ‘organ’ with endocrine function and the bioactive metabolites produced by it can affect the physiological role of the host. With deepening researches in recent years, clinical data indicated that the GM has a significant effect on the occurrence and development of cardiovascular diseases (CVD). This article systematically elaborated the relationship between metabolites of GM and its effects, the relationship between intestinal dysbacteriosis and cardiovascular risk factors, coronary heart disease, myocardial infarction, heart failure and hypertension and the possible pathogenic mechanisms. Regulating the GM is supposed to be a potential new therapeutic target for CVD.     

The role of intestinal microbiota in cardiovascular disease

Accumulating evidence has indicated that intestinal microbiota is involved in the development of various human diseases, including cardiovascular diseases (CVDs). In the recent years, both human and animal experiments have revealed that alterations in the composition and function of intestinal flora, recognized as gut microflora dysbiosis, can accelerate the progression of CVDs. Moreover, intestinal flora metabolizes the diet ingested by the host into a series of metabolites, including trimethylamine N‐oxide, short chain fatty acids, secondary bile acid and indoxyl sulfate, which affects the host physiological processes by activation of numerous signalling pathways. The aim of this review was to summarize the role of gut microbiota in the pathogenesis of CVDs, including coronary artery disease, hypertension and heart failure, which may provide valuable insights into potential therapeutic strategies for CVD that involve interfering with the composition, function and metabolites of the intestinal flora.     

Microbial Metabolites and Intestinal Stem Cells Tune Intestinal Homeostasis

Microorganisms that colonize the gastrointestinal tract, collectively known as the gut microbiota, are known to produce small molecules and metabolites that significantly contribute to host intestinal development, functions, and homeostasis. Emerging insights from microbiome research reveal that gut microbiota‐derived signals and molecules influence another key player maintaining intestinal homeostasis—the intestinal stem cell niche, which regulates epithelial self‐renewal. In this review, the literature on gut microbiota‐host crosstalk is surveyed, highlighting the effects of gut microbial metabolites on intestinal stem cells. The production of various classes of metabolites, their actions on intestinal stem cells are discussed and, finally, how the production and function of metabolites are modulated by aging and dietary intake is commented upon.     

The gut microbiota and its interactions with cardiovascular disease

The intestine is colonized by a considerable community of microorganisms that cohabits within the host and plays a critical role in maintaining host homeostasis. Recently, accumulating evidence has revealed that the gut microbial ecology plays a pivotal role in the occurrence and development of cardiovascular disease (CVD). Moreover, the effects of imbalances in microbe–host interactions on homeostasis can lead to the progression of CVD. Alterations in the composition of gut flora and disruptions in gut microbial metabolism are implicated in the pathogenesis of CVD. Furthermore, the gut microbiota functions like an endocrine organ that produces bioactive metabolites, including trimethylamine/trimethylamine N-oxide, short-chain fatty acids and bile acids, which are also involved in host health and disease via numerous pathways. Thus, the gut microbiota and its metabolic pathways have attracted growing attention as a therapeutic target for CVD treatment. The fundamental purpose of this review was to summarize recent studies that have illustrated the complex interactions between the gut microbiota, their metabolites and the development of common CVD, as well as the effects of gut dysbiosis on CVD risk factors. Moreover, we systematically discuss the normal physiology of gut microbiota and potential therapeutic strategies targeting gut microbiota to prevent and treat CVD.     

The role of intestinal microbiota and its metabolites in intestinal and extraintestinal organ injury induced by intestinal ischemia reperfusion injury

Intestinal ischemia/reperfusion (I/R) is a common pathophysiological process in clinical severe patients, and the effect of intestinal I/R injury on the patient''s systemic pathophysiological state is far greater than that of primary intestinal injury. In recent years, more and more evidence has shown that intestinal microbiota and its metabolites play an important role in the occurrence, development, diagnosis and treatment of intestinal I/R injury. Intestinal microbiota is regulated by host genes, immune response, diet, drugs and other factors. The metabolism and immune potential of intestinal microbiota determine its important significance in host health and diseases. Therefore, targeting the intestinal microbiota and its metabolites may be an effective therapy for the treatment of intestinal I/R injury and intestinal I/R-induced extraintestinal organ injury. This review focuses on the role of intestinal microbiota and its metabolites in intestinal I/R injury and intestinal I/R-induced extraintestinal organ injury, and summarizes the latest progress in regulating intestinal microbiota to treat intestinal I/R injury and intestinal I/R-induced extraintestinal organ injury.     

Gut microbiota,host health,and polysaccharides

The intestinal microbiota is a complicated ecosystem that influences many aspects of host physiology (i.e. diet, disease development, drug metabolism, and regulation of the immune system). It also exhibits spatial patterning and temporal dynamics. In this review, the effects of internal and external (environmental) factors on intestinal microbiota are discussed. We describe the roles of the gut microbiota in maintaining intestinal and immune system homeostasis and the relationship between gut microbiota and diseases. In particular, the contributions of polysaccharides, as the most abundant diet components in intestinal microbiota and host health are presented. Finally, perspectives for research avenues relating to gut microbiota are also discussed.     

Dendritic cells in intestinal immune regulation

A breakdown in intestinal homeostasis can result in chronic inflammatory diseases of the gut including inflammatory bowel disease, coeliac disease and allergy. Dendritic cells, through their ability to orchestrate protective immunity and immune tolerance in the host, have a key role in shaping the intestinal immune response. The mechanisms through which dendritic cells can respond to environmental cues in the intestine and select appropriate immune responses have until recently been poorly understood. Here, we review recent work that is beginning to identify factors responsible for intestinal conditioning of dendritic-cell function and the subsequent decision between tolerance and immunity in the intestine.     

肠道微生物与子宫内膜癌相关危险因素的研究进展

子宫内膜癌（endometrial carcinoma,EC）是一种常见的妇科恶性肿瘤,以雌激素升高、肥胖和胰岛素抵抗等临床表现为主要特征,这些特征影响了EC的进展及预后。肠道菌群是由大量微生物组成的复杂系统,它们维持着人体各系统的稳态并产生一些代谢产物来对机体发挥作用。但因其数量巨大,在菌群失调时可导致宿主生理机能发生紊乱,微生物产生的毒性代谢物参与炎症并增加与肿瘤相关的通路,影响机体的吸收代谢、肿瘤进展和恶化等。随着基因检测技术的发展,越来越多的证据表明肠道微生物与EC的危险因素存在相关性,能促进EC的发生发展。本文主要介绍肠道微生物对EC发生发展的影响,重点探讨肠道微生物与EC相关危险因素间的关系,以期为EC的治疗与预后管理提供新思路。