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1.
肠道菌群与人体通过广泛信息交流形成互惠共生关系。肠道菌群结构稳定性、菌种多样性和微生态平衡性使其成为人体更易接触和调控的"生理中心",深刻影响人体健康。适宜运动可通过优化肠道菌群,促进宿主肠道微生态健康。以肠道菌群为靶点的运动健康促进研究,为运动与人体健康和疾病研究呈现出新领域。基于宏基因组学、宏转录组学等微生态研究技术,揭示与人体疾病相关的肠道菌群失调,鉴定出疾病相关的特定菌群种类及功能,使得以肠道菌群为靶点的运动精准干预人体健康成为可能。  相似文献   

2.
肠道菌群对维持人体健康发挥着重要的作用。肠道菌群编码的基因数量是人体基因的100多倍,被称之为人体的第二基因组。人体的基因难于改变,而肠道菌群组成的改变则相对容易。本文介绍了影响肠道菌群的几大核心因素,以期能深入理解不同个体肠道菌群的异同,为相关研究提供参考。  相似文献   

3.
细菌耐药影响肠道菌群及其宿主免疫调控   总被引:2,自引:0,他引:2       下载免费PDF全文
抗生素在养殖业、医疗业及制药业的广泛应用导致环境中的细菌耐药性日益严重,环境中的抗生素及耐药细菌一旦进入人体肠道,将破坏肠道菌群稳态,对人体健康造成威胁,而残存于饮食中的环境污染物则加剧了细菌耐药造成的人体健康影响。文中在总结大量文献的基础上,阐述了细菌耐药对人体和动物肠道菌群的影响机制及其相关的机体免疫调控,以环境中影响人体肠道菌群获得耐药性的来源作为切入点,阐述抗生素和耐药细菌进入人体肠道后对人体肠道菌群结构和耐药基因组成的影响,以及与人体免疫和免疫调节相关疾病之间的相关机制,并对今后的研究方向进行了展望。  相似文献   

4.
<正>肠道微生物菌群可以参与人体新陈代谢,与健康和各种疾病密切相关,其中细菌数量是人体细胞总数的10倍。之前研究报道称,人体肠道中大约存在1000到1150种细菌,平均每个个体内约含有160种优势菌种。这些肠道菌群与人体互利共生,并为人体产生有益的物质,保护人体健康。饮食也会导致肠道菌群的结构失衡,从而引发肥胖、肠炎和糖尿等疾病。迄今为止最具代表性、最高质量、近乎完整的人类肠道微生物参考基因集数据库。  相似文献   

5.
人体肠道作为一个多元化的微生态系统,其中共生着100多万亿个微生物菌群,约有1 000多种,是人体细胞的10倍。肠道微生物固有的微生物基因有300多万个,是人体基因的100多倍,这些微生物基因帮助人体微生物适应多变的环境,与人类相互作用,对人类健康产生了巨大影响,其中有积极的作用,同时又伴随着潜在的威胁。总结了肠道微生物菌群与消化道肿瘤的关系,从肠道菌群的多样性、影响因素及其作用机制展开综述,以期为开展肠道微生物的研究提供参考。  相似文献   

6.
正正常成人胃肠道菌群有1 000余种,总量达1013-14[1],10倍于人体细胞总量,人体正常肠道菌群的基因总和是人体自身基因的100~150倍[2]。肠道是人体最大的消化器官,同时也是最大的免疫器官和代谢器官。儿童肠道菌群的定植与建立对出生后消化系统、免疫系统和代谢等发育和成熟具有重大作用。肠道菌群紊乱与感染性疾病、免疫性疾病和代谢性疾病的发生和发展具有密切的关系。近5年来,粪菌移  相似文献   

7.
肠道微生物对人体健康和疾病发生发展都有着重要的影响。健康的肠道菌群不仅可以保护宿主免受病原菌的侵袭,还可以参与人体多项生理过程,包括生物活性代谢物的产生、免疫调节、糖脂代谢、维持体内平衡等。膳食中的脂肪、蛋白质和碳水化合物作为主要的营养素,在为人类机体提供能量的同时,也对肠道菌群的组成产生重要影响。精准营养旨在结合膳食指南,根据不同个体对营养的需求以及自身基因、肠道菌群的差异,提供科学的个性化膳食建议,以期实现对疾病的预防和控制。但精准营养的发展还存在着诸多方法学上的局限。本文主要回顾了肠道菌群、膳食与健康三者之间的相互关系,指出肠道菌群在精准营养与健康研究中的重要作用和发展前景,重点提出在人群队列水平将人工智能算法应用于肠道微生物组等多组学大数据的必要性及其对精准营养研究的关键作用。  相似文献   

8.
人体肠道内含有大量的微生物,直接参与了机体的各种代谢活动,与人体健康密切相关。研究显示肠道菌群的构成和稳定受到诸多宿主和环境因素的影响,其中饮食因素起着至关重要的作用。特别是西方高脂饮食方式造成肠道菌群结构改变,从而导致一些慢性、非传染性和免疫相关性疾病的发生。在过去的几十年中,肠道菌群在人体健康中的作用越来越受到关注。不同饮食结构可以对肠道菌群的组成和多样性产生重要的影响。在这篇综述中,我们总结了肠道微生物与人体健康之间的关系以及益生菌在饮食中的作用,为指导和建立健康饮食结构提供理论指导,为相应疾病的防治提供参考。  相似文献   

9.
<正>近日,浙江大学医学院附属第一医院传染病诊治国家重点实验室、感染性疾病诊治协同创新中心主任李兰娟院士及其科研团队,找到了汉族人和肝硬化相关的肠道菌群的遗传特征,为检测晚期肝疾病提供了方法。该研究成果在学术期刊《自然》发表。目前,部分病毒性肝炎及脂肪性、酒精性、药物性、免疫性肝病患者会经历肝炎、肝硬化、肝癌"三部曲"。尽管有些研究表明,肠道微生物的改变在终末期肝硬化并发症中起重要作用,但一直缺乏肠道菌群和肝脏病变的确切关联证据。李兰娟院士及其科研团队通过收集181个来自于中国人肠道菌群的样本,其中包括98个中国肝硬化患者及83个健康中国志愿者的粪便样本,用宏基因组学的研究方法,开展了肝硬化肠道菌群的深度测序及关联分析研究,从中获得269万个非冗余的人体肠道微生物菌群的基因集,  相似文献   

10.
当前慢病高发的现实对"健康中国2030"战略目标的实现提出了巨大挑战。虽然众多医疗机构和政府管理部门付出巨大努力,然而如果仍然沿袭现有慢病防控模式和医疗改革理念,恐怕很难在近期内实现慢病防控的突破,迫切需要引入新思路,才有可能破解慢病高发这个难题。根据近年来国内外大量报道人体共生微生物尤其是肠道菌群与人体多种慢病之间存在密切相关性甚至因果性的研究进展,以及在此启发下我们实验室通过大量研究发现"饥饿源于菌群",结合诸多文献报道证明通过调控肠道菌群微生态可改善多种慢病,为"慢病源于菌群"提供了重要依据,从而提出"医学遗传学2.0"(Medical genetics 2.0, MG2.0)的概念,其核心思想是将复杂性疾病(主要指慢病)的致病因素优先归因于人体共生微生物尤其是肠道菌群基因组异常,而人类基因组异常则是跟随前者发生顺应性改变的结果,即人体共生微生物基因组异常是慢病的主要矛盾,人类自身的基因组异常是慢病的次要矛盾,两套基因组通过联立交互作用,最终导致人体慢病持续发展。如果只是通过纠正人类基因组异常,而忽视了纠正菌群基因组异常,则难以从根本上治疗慢病,因为异常的菌群基因组仍然会持续影响人体健康。因此,在慢病防控方面,建议医学遗传学领域的研究重点可向肠道菌群等人体共生微生物领域进行深化,广泛开展以人体共生微生物尤其是肠道菌群基因组为主、人类基因组为辅的人菌双基因组关联分析研究,建立不同慢病的菌群图谱(含基因组学、转录组学、蛋白质组学、代谢组学以及生命组学等相关研究),并研究纠正异常菌群图谱的方法(含靶向肠道菌群的新药研发),为慢病防控找到新出路。  相似文献   

11.
Genetically-engineered animals are known to be useful in clarifying the functions of many genes and as animal models for human diseases. However, it has been widely reported that pathophysiology is not expressed in these animals when they become germfree or SPF animals, i.e., the pathophysiology is not the result of genes alone and a combination of gene function and intestinal flora as an environmental factor are necessary. It is important to determine the roles of each of these two factors by pathophysiological analysis. Gnotobiotic mice were produced by establishment of specified bacterial species in germfree animals to form the intestinal flora of SPF animals and they were placed in barrier facilities. Measures have been taken against infections by bacteria such as Pseudomonas aeruginosa and Enterobacter cloacae. In addition, gnotobiotic mice with a highly normal physiology are required. Analysis of the effects of each bacterial species and combinations of bacteria on in vivo functions, i.e., the cross-talk between the host and intestinal flora, is essential in the creation of better laboratory animals. Monitoring of the intestinal flora, a key factor in the colonies produced, is a topic for future research.  相似文献   

12.
The complex interplay between symbiotic bacteria and host immunity plays a key role in shaping intestinal homeostasis and maintaining host health. Paneth cells, as one of the major producers of antimicrobial peptides in the intestine under steady-state conditions, play a vital role in regulating intestinal flora. Many studies on inflammatory bowel disease (IBD)-associated genes have put Paneth cells at the center of IBD pathogenesis. In this perspective, we focus on mechanistic studies of different cellular processes in Paneth cells that are regulated by various IBD-associated susceptibility genes, and we discuss the hypothesis that Paneth cells function as the central hub for sensing and regulating intestinal flora in the maintenance of intestinal homeostasis.  相似文献   

13.
The small and large intestines contain an abundance of luminal antigens derived from food products and enteric microorganisms. The function of intestinal epithelial cells is tightly regulated by several factors produced by enteric bacteria and the epithelial cells themselves. Epithelial cells actively participate in regulating the homeostasis of intestine, and failure of this function leads to abnormal and host-microbial interactions resulting in the development of intestinal inflammation. Major determinants of host susceptibility against luminal commensal bacteria include genes regulating mucosal immune responses, intestinal barrier function and microbial defense. Of note, it has been postulated that commensal bacterial adhesion and invasion on/into host cells may be strongly involved in the pathogenesis of inflammatory bowel disease (IBD). During the intestinal inflammation, the composition of the commensal flora is altered, with increased population of aggressive and detrimental bacteria and decreased populations of protective bacteria. In fact, some pathogenic bacteria, including Adherent-Invasive Escherichia coli, Listeria monocytogenes and Vibrio cholerae are likely to initiate their adhesion to the host cells by expressing accessory molecules such as chitinases and/or chitin-binding proteins on themselves. In addition, several inducible molecules (e.g., chitinase 3-like 1, CEACAM6) are also induced on the host cells (e.g. epithelial cells, lamina proprial macrophages) under inflammatory conditions, and are actively participated in the host-microbial interactions. In this review, we will summarize and discuss the potential roles of these important molecules during the development of acute and chronic inflammatory conditions.  相似文献   

14.
15.
Homologous rotaviruses (RV) are, in general, more virulent and replicate more efficiently than heterologous RV in the intestine of the homologous host. The genetic basis for RV host range restriction is not fully understood and is likely to be multigenic. In previous studies, RV genes encoding VP3, VP4, VP7, nonstructural protein 1 (NSP1), and NSP4 have all been implicated in strain- and host species-specific infection. These studies used different RV strains, variable measurements of host range, and different animal hosts, and no clear consensus on the host range restriction determinants emerged. We used a murine model to demonstrate that enteric replication of murine RV EW is 1,000- to 10,000-fold greater than that of a simian rotavirus (RRV) in suckling mice. Intestinal replication of a series of EW × RRV reassortants was used to identify several RV genes that influenced RV replication in the intestine. The role of VP4 (encoded by gene 4) in enteric infection was strain specific. RRV VP4 reduced murine RV infectivity only slightly; however, a reassortant expressing VP4 from a bovine RV strain (UK) severely restricted intestinal replication in the suckling mice. The homologous murine EW NSP1 (encoded by gene 5) was necessary but not sufficient for promoting efficient enteric growth. Efficient enteric replication required a constellation of murine genes encoding VP3, NSP2, and NSP3 along with NSP1.  相似文献   

16.
Abrams, Gerald D. (The University of Michigan Medical School, Ann Arbor), and Jane E. Bishop. Effect of the normal microbial flora on the resistance of the small intestine to infection. J. Bacteriol. 92:1604-1608. 1966.-Mucosal structure in the small intestine is known to be influenced by the normal microbial flora. This suggests that mucosal resistance to invasion by enteric pathogens might also be affected by the flora. To assess this possibility, germ-free and conventional mice were challenged with Salmonella typhimurium, and both the growth of organisms within the intestinal lumen and the translocation to mesenteric lymph nodes were studied quantitatively. There were significantly more organisms 24 hr after intragastric challenge in the mesenteric nodes of germ-free animals than in those of conventional ones. However, since intraluminal growth in the intestine was also greater in germ-free animals, no conclusion could be drawn about mucosal resistance per se. Results were similar when the challenge was intraduodenal. However, when intestinal emptying was prevented by ileal ligation before challenge, both intraluminal growth and translocation of S. typhimurium were equal in the two groups of mice. It is concluded from these data, as well as from preliminary dye studies of intestinal motility, that the normal flora does not influence mucosal resistance directly, but may alter enteric infection by affecting intestinal emptying.  相似文献   

17.
肠道菌群对宿主免疫系统的建立和发育起着重要的作用,与宿主的生理、病理等密切相关,对机体抗病毒作用具有一定的影响。病毒感染影响宿主肠道微生物群落,进而影响宿主机体营养物质的代谢及细胞免疫功能。本研究着重综述病毒感染对宿主肠道微生态及免疫的影响。  相似文献   

18.
Sawires YS  Songer JG 《Anaerobe》2006,12(1):23-43
Clostridium perfringens is an important pathogen in veterinary and medical fields. Diseases caused by this organism are in many cases life threatening or fatal. At the same time, it is part of the ecological community of the intestinal tract of man and animals. Virulence in this species is not fully understood and it does seem that there is erratic distribution of the toxin/enzyme genes within C. perfringens population. We used the recently developed multiple-locus variable-number tandem repeat analysis (MLVA) scheme to investigate the evolution of virulence and population structure of this species. Analysis of the phylogenetic signal indicates that acquisition of the major toxin genes as well as other plasmid-borne toxin genes is a recent evolutionary event and their maintenance is essentially a function of the selective advantage they confer in certain niches under different conditions. In addition, it indicates the ability of virulent strains to cause disease in different host species. More interestingly, there is evidence that certain normal flora strains are virulent when they gain access to a different host species. Analysis of the population structure indicates that recombination events are the major tool that shapes the population and this panmixia is interrupted by frequent clonal expansion that mostly corresponds to disease processes. The signature of positive selection was detected in alpha toxin gene, suggesting the possibility of adaptive alleles on the other chromosomally encoded determinants. Finally, C. perfringens proved to have a dynamic population and availability of more genome sequences and use of comparative proteomics and animal modeling would provide more insight into the virulence of this organism.  相似文献   

19.
Although the intestinal flora in animals plays an important role in health and disease, there is little direct information regarding the role of the human intestinal flora. By inoculating germfree animals with human faeces, the major components of the human flora can be transferred into the ex-germfree animals, i.e. human flora-associated (HFA) animals. HFA animals therefore provide a stable model for studying the ecosystem and metabolism of the human intestinal flora. Results with HFA animals suggest the role of the human intestinal flora is somewhat different from the role of the animal flora in conventional experimental animals. Studies using HFA animals, therefore, will provide much needed information on the precise role of the intestinal flora in relation to humans. HFA animals also can be used as models to investigate the interactions between the human intestinal flora, host factors, dietary manipulations, and therapeutics, such as probiotics, prebiotics, and antibiotics.  相似文献   

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