马齿苋多糖对肠道微生态失调小鼠的调整作用研究

目的研究应用马齿苋多糖对肠道微生态失调小鼠进行调整治疗,达到从微生态学角度防治感染的目的。方法应用林可霉素灌胃建立肠道微生态失调小鼠模型,然后用马齿苋多糖进行治疗,同时设正常对照组、阳性对照组和阴性对照组,于给药7 d后处死小鼠,进行肠道菌群定量、肠内容物挥发性脂肪酸检测及肠黏膜电镜观察。结果林可霉素灌胃3 d后,小鼠肠道菌群失调,肠内容物挥发性脂肪酸含量明显下降,肠黏膜损伤严重。持续7 d治疗后,治疗组小鼠肠道双歧杆菌和乳酸杆菌数量明显上升,肠内容物挥发性脂肪酸含量明显上升,损伤的肠黏膜基本修复。结论应用林可霉素可以成功建立肠道微生态失调动物模型;马齿苋多糖具有扶植肠道正常菌群生长,调整菌群失调,防治感染的作用,是理想的中药微生态调节剂。     

红花多糖对肠道微生态失调小鼠肠黏膜sIgA、血浆内毒素和肠道菌群的影响

目的 研究红花多糖对肠道微生态失调小鼠的调节作用,探讨红花多糖改善微生态失调与肠黏膜免疫、血浆内毒素及肠道菌群的关系.方法 应用盐酸林可霉素灌胃建立肠道微生态失调小鼠模型,然后用红花多糖进行治疗,同时设正常对照组(n=5)、自然恢复组(n=5)和丽珠肠乐组(n=5).于给药7d后处死小鼠,进行肠黏膜sIgA、血浆内毒素...     

肠道菌群影响黏膜屏障结构与功能的研究进展

肠道黏膜屏障具有防止致病性抗原侵入、维护肠道健康的功能。而肠道菌群是肠道黏膜屏障的重要构成部分,肠道菌群失调会导致肠道黏膜屏障的损伤,引起炎性肠病、肠易激综合征及肝、肾等多种疾病的发生发展。因此,本文从肠道黏膜的结构与功能及肠道菌群对其的影响等方面归纳总结肠道菌群对屏障系统的调控作用,从调节肠道微生态平衡、促进黏液分泌、影响紧密连接和肠道上皮通透性、激发肠黏膜免疫、调控肠上皮凋亡、影响肠上皮DNA稳定性及产生特殊代谢产物等方面阐述其作用机制,为临床胃肠道疾病及其并发症的治疗提供新的思路和方法。     

肠道微生态在肝癌诊疗应用中的研究进展

肠道微生态是由数量巨大且结构复杂的肠道菌群与肠黏膜屏障组成,参与机体多种重要生理功能,与多种疾病密切相关。由于肠道与肝脏有着密切而特殊的关系,肠道微生态可通过肠―肝循环及其与宿主的相互作用来调节肝脏疾病的进展。肠道微生态失调与肝癌进展密切相关,肠道中关键功能菌可作为肝癌早期预防、诊断和治疗的新的预测标记物与新的治疗靶点。本文将对肠道微生态在肝癌发病机制中的作用以及基于肠道微生态理论的多种肝癌防治策略进行综述。     

八珍制剂对60Co辐射小鼠微生态失调的促恢复作用

目的观察中药八珍制剂对60Co辐射小鼠微生态失调的调整作用.方法 60Co辐射昆明种小鼠制成微生态失调模型,用中药八珍制剂对其进行调整,检测肠道膜菌群与腔菌群中双歧杆菌、乳酸杆菌、肠杆菌、肠球菌及肝脏细菌易位数量,血浆内毒素水平,小肠黏膜中二胺氧化酶的活性和丙二醛的含量等指标,观测中药对辐射性微生态失调的调整作用.结果:中药八珍制剂具有调整小鼠肠道菌群失调,降低肠道菌易位和血浆内毒素水平,减少丙二醛含量,升高肠黏膜中二胺氧化酶的活性.中药治疗组各项指标与自然恢复组相比,差异均有显著性( P<0.001或P<0.01或P<0.05).结论八珍制剂对60Co辐射小鼠微生态失调有促恢复作用.     

黄芪多糖对微生态调节作用的物质基础研究初探

目的探讨黄芪多糖微生态调节作用的活性成分。方法采用水提醇沉法提取黄芪总多糖,三氯乙酸除蛋白,纯化后的多糖分别过中空纤维膜,分子量截留值为150、100、50、20、10和6 kDa,得到不同分子量级别的多糖。应用盐酸林可霉素灌胃建立肠道微生态失调小鼠模型,用不同分子量的7组黄芪多糖进行治疗,同时设正常对照组、阳性对照组和阴性对照组,于给药7 d后处死小鼠,进行各种药效学指标的测定。结果分子量由大到小的7组黄芪多糖占总糖比例依次为59.1%、0.9%、3.4%、9.4%、2.4%、5.3%和19.5%;7组多糖均有不同程度的扶植有益菌、抑制有害菌的作用,其中10～6 kDa多糖调节小鼠肠道微生态菌群平衡效果最好。结论经过药效学实验筛选出10～6kDa黄芪多糖对调节小鼠肠道菌群平衡具有重要作用,初步阐明了黄芪多糖微生态调节作用的物质基础。     

NLRP6炎症小体与肠道微生态研究进展

NLRP6炎症小体作为炎症反应的核心识别环节,由PRRs、ASC、Caspase三部分组成,可激活下游IL-1β、IL-18等炎症分子。肠道微生态主要由肠道内结构复杂的微生物、种类繁多的代谢物和肠道黏膜屏障组成,参与机体多种重要生命功能,与多种疾病发生发展密切相关。NLRP6炎症小体广泛分布于肠道组织中,可识别肠道内多种危险信号,进而与众多下游信号通路关联,调控肠道内微生物组成和肠道黏膜屏障,从而调控疾病进展。此外,肠道微生物菌群或其代谢产物可直接激活NLRP6炎症小体,也可通过肠-肝循环刺激肝脏内NLRP6炎症小体,对维持肠道微生态平衡及宿主-微生物相互作用至关重要。基于NLRP6炎症小体与肠道微生态之间的相互调控机制,靶向NLRP6炎症小体调节肠道微生态失衡,成为与肠道微生态失衡相关疾病治疗的新思路。文章就NLRP6炎症小体的组成、分布与激活,NLRP6炎症小体与肠道微生物、代谢产物、肠道黏膜屏障相互调控机制进行综述,为临床治疗肠道微生态失衡相关疾病提供更多研究思路。     

八珍制剂对~(60)Co辐射小鼠微生态失调的促恢复作用

目的　观察中药八珍制剂对60 Co辐射小鼠微生态失调的调整作用。方法　60 Co辐射昆明种小鼠制成微生态失调模型 ,用中药八珍制剂对其进行调整 ,检测肠道膜菌群与腔菌群中双歧杆菌、乳酸杆菌、肠杆菌、肠球菌及肝脏细菌易位数量 ,血浆内毒素水平 ,小肠黏膜中二胺氧化酶的活性和丙二醛的含量等指标 ,观测中药对辐射性微生态失调的调整作用。结果 :中药八珍制剂具有调整小鼠肠道菌群失调 ,降低肠道菌易位和血浆内毒素水平 ,减少丙二醛含量 ,升高肠黏膜中二胺氧化酶的活性。中药治疗组各项指标与自然恢复组相比 ,差异均有显著性(P <0 .0 0 1或P <0 .0 1或P <0 .0 5 )。结论　八珍制剂对60 Co辐射小鼠微生态失调有促恢复作用     

肠道微生态与非消化系统疾病的研究进展

人体肠道微生态系统是人体微生态系统中最大最复杂的一部分,参与机体代谢、免疫等各方面的生理作用。由于内外源性的病理因素导致肠道微生态的破坏可能会引起人体疾病。随着肠道微生态与消化道疾病研究的不断深入,越来越多的学者开始关注肠道微生态与非消化道疾病的相关性。近年来大量研究表明,肠道微生态与肥胖、神经精神病、皮肤病、心脑血管疾病、消化道外肿瘤、感染性疾病和自身免疫病等非消化系统疾病具有相关性。微生态制剂和粪菌移植可以通过调节肠道微生态平衡参与这类疾病的预防和治疗。肠道微生态系统与消化系统疾病的相关性已被广泛研究和阐述,本文侧重对肠道微生态与非消化系统疾病的研究进展进行综述。     

香菇多糖对溃疡性结肠炎大鼠肠道微生态失调的调整作用研究

目的研究香菇多糖通过扶植肠道正常菌群生长,控制内毒素易位,对溃疡性结肠炎大鼠肠道微生态失调进行调整,从微生态学角度防治溃疡性结肠炎。方法 Wistar大白鼠48只,随机取8只作为正常对照组,其余40只造模。之后以香菇多糖和丽珠肠乐灌胃,14 d后处死。取肠内容物、血液,分别进行细菌培养、检测挥发性脂肪酸、内毒素。结果经过香菇多糖和丽珠肠乐治疗后,大鼠肠道双歧杆菌、乳酸杆菌的数量明显上升,大肠埃希菌、肠球菌的数量明显下降;肠内容物挥发性脂肪酸含量显著上升;血中内毒素含量显著下降。结论香菇多糖和丽珠肠乐均具有扶植正常菌群生长,调整菌群失调,提高机体免疫力,防治溃疡性结肠炎的作用;香菇多糖和丽珠肠乐联合应用效果更佳。     

肠道上皮与肠道微生物相互作用的研究现状

肠道上皮是肠上皮细胞及其分泌物有机构成的黏膜界面。随着技术的进步和对肠道菌群作用的逐渐重视,研究者对肠道上皮与肠道微生物相互作用的认识也不断深入。研究表明,肠道上皮调节并维持肠道微生物的定殖与分布,肠道微生物也影响肠道上皮的多种屏障功能,二者通过一系列细胞分子机制紧密联系,共同维持肠道稳态。此外,其过程中产生的宿主-肠道菌群共代谢物被发现可以反映宿主的生理病理状态,作为指标被应用于临床疾病诊断、治疗效果评估和预后推测。本文基于近年的研究,综述了肠道上皮与肠道微生物的相互作用及其细胞分子机制,为进一步研究和临床应用总结了理论基础,并探讨了未来可能的研究方向。     

多糖与肠道菌群相互作用及其构效关系研究进展

肠道菌群是一个复杂的生态系统,影响宿主的饮食、疾病发展、药物代谢和免疫系统调节等诸多生理方面。多糖广泛存在于动物、植物及微生物中,具有多种生理活性。肠道菌群与多糖相互作用,消化难以消化的多糖,多糖作为肠道菌群的重要能量来源,促进益生菌增殖。肠道菌群紊乱导致疾病的发生,多糖通过调节肠道菌群改善疾病。随着“人类微生物组计划”的启动和国内外学者对肠道菌群的深入研究,多糖与肠道菌群的关系逐渐清晰,但多糖的结构与肠道菌群之间的关系还有待进一步探究。因此,本文综述了多糖与肠道菌群的相互作用,并通过调节肠道菌群的组成来改善疾病,以及从多糖的分子量、糖苷键、单糖组成三方面探讨多糖与肠道菌群的构效关系,同时对未来研究的方向进行展望,以期为治疗疾病的深入研究提供重要参照和建议。     

Gut dysbacteriosis and intestinal disease: mechanism and treatment

The gut microbiome functions like an endocrine organ, generating bioactive metabolites, enzymes or small molecules that can impact host physiology. Gut dysbacteriosis is associated with many intestinal diseases including (but not limited to) inflammatory bowel disease, primary sclerosing cholangitis-IBD, irritable bowel syndrome, chronic constipation, osmotic diarrhoea and colorectal cancer. The potential pathogenic mechanism of gut dysbacteriosis associated with intestinal diseases includes the alteration of composition of gut microbiota as well as the gut microbiota–derived signalling molecules. The many correlations between the latter and the susceptibility for intestinal diseases has placed a spotlight on the gut microbiome as a potential novel target for therapeutics. Currently, faecal microbial transplantation, dietary interventions, use of probiotics, prebiotics and drugs are the major therapeutic tools utilized to impact dysbacteriosis and associated intestinal diseases. In this review, we systematically summarized the role of intestinal microbiome in the occurrence and development of intestinal diseases. The potential mechanism of the complex interplay between gut dysbacteriosis and intestinal diseases, and the treatment methods are also highlighted.     

The root microbiome: Community assembly and its contributions to plant fitness

The root microbiome refers to the community of microbes living in association with a plant's roots, and includes mutualists, pathogens, and commensals. Here we focus on recent advances in the study of root commensal community which is the major research object of microbiome-related researches. With the rapid development of new technologies, plant–commensal interactions can be explored with unprecedented breadth and depth. Both the soil environment and the host plant drive commensal community assembly. The bulk soil is the seed bank of potential commensals, and plants use root exudates and immune responses to build healthy microbial communities from the available microbes. The plant microbiome extends the functional system of plants by participating in a variety of processes, including nutrient absorption, growth promotion, and resistance to biotic and abiotic stresses. Plants and their microbiomes have evolved adaptation strategies over time. However, there is still a huge gap in our understanding of the regulatory mechanisms of plant–commensal interactions. In this review, we summarize recent research on the assembly of root microbial communities and the effects of these communities on plant growth and development, and look at the prospects for promoting sustainable agricultural development through the study of the root microbiome.     

微生物组学对植物病害微生物防治研究的启示

植物病害的微生物防治研究主要集中在植物、病原菌和生防菌三者的互作关系上,相对忽视了植物微生物组/群的作用。越来越多的研究表明,植物内生微生物、根围土壤微生物和叶围微生物均不同程度地参与了植物防病的机制。为了更好地了解相关进展,本文选择部分代表性研究,详述了植物微生物组/群的构成,并结合案例介绍了植物微生物组/群对寄主植物的防/致病作用、对植物病原菌致病性的影响,以及施用生防菌对植物微生物组/群的影响。微生物组学的发展为生防机制领域提出了新的研究思路,有利于发现更加科学的防治手段。     

肠道菌群与肾脏疾病相关性研究进展

人体是一个有机的整体,不同系统之间存在着相互影响。近年来,随着科学的不断发展,肠道菌群与人体健康的关系也逐渐受到重视。肠道菌群虽然居住于肠道,但其作用已经不仅仅局限于消化系统。通过对人体代谢和免疫功能的影响,肠道菌群对人体产生的作用是全身性的。肾脏是体内代谢产物排泄的主要器官,也是免疫复合物沉积的重要部位。因此,肠道菌群在肾脏疾病发展和治疗中都起着至关重要的作用。现如今,两者的关系已经成为科学研究的热点话题。本文总结了近5年的文献,从中西医的角度,针对肠道菌群与肾脏疾病之间的相互关系作一综述。     

Prolonged antibiotic treatment induces a diabetogenic intestinal microbiome that accelerates diabetes in NOD mice

Accumulating evidence supports that the intestinal microbiome is involved in Type 1 diabetes (T1D) pathogenesis through the gut-pancreas nexus. Our aim was to determine whether the intestinal microbiota in the non-obese diabetic (NOD) mouse model played a role in T1D through the gut. To examine the effect of the intestinal microbiota on T1D onset, we manipulated gut microbes by: (1) the fecal transplantation between non-obese diabetic (NOD) and resistant (NOR) mice and (2) the oral antibiotic and probiotic treatment of NOD mice. We monitored diabetes onset, quantified CD4+T cells in the Peyer''s patches, profiled the microbiome and measured fecal short-chain fatty acids (SCFA). The gut microbiota from NOD mice harbored more pathobionts and fewer beneficial microbes in comparison with NOR mice. Fecal transplantation of NOD microbes induced insulitis in NOR hosts suggesting that the NOD microbiome is diabetogenic. Moreover, antibiotic exposure accelerated diabetes onset in NOD mice accompanied by increased T-helper type 1 (Th1) and reduced Th17 cells in the intestinal lymphoid tissues. The diabetogenic microbiome was characterized by a metagenome altered in several metabolic gene clusters. Furthermore, diabetes susceptibility correlated with reduced fecal SCFAs. In an attempt to correct the diabetogenic microbiome, we administered VLS#3 probiotics to NOD mice but found that VSL#3 colonized the intestine poorly and did not delay diabetes. We conclude that NOD mice harbor gut microbes that induce diabetes and that their diabetogenic microbiome can be amplified early in life through antibiotic exposure. Protective microbes like VSL#3 are insufficient to overcome the effects of a diabetogenic microbiome.     

Microbiome predators in changing soils

Microbiome predators shape the soil microbiome and thereby soil functions. However, this knowledge has been obtained from small-scale observations in fundamental rather than applied settings and has focused on a few species under ambient conditions. Therefore, there are several unaddressed questions on soil microbiome predators: (1) What is the role of microbiome predators in soil functioning? (2) How does global change affect microbiome predators and their functions? (3) How can microbiome predators be applied in agriculture? We show that there is sufficient evidence for the vital role of microbiome predators in soils and stress that global changes impact their functions, something that urgently needs to be addressed to better understand soil functioning as a whole. We are convinced that there is a potential for the application of microbiome predators in agricultural settings, as they may help to sustainably increase plant growth. Therefore, we plea for more applied research on microbiome predators.     

肠道微生物与结直肠癌

结直肠癌(colorectal cancer, CRC)是最常见的恶性肿瘤之一,严重威胁着人类健康。肠道微生态作为人体内最复杂、最庞大的微生态系统,与CRC密切相关。CRC患者的肠道微生物群落多样性构成能调节CRC疾病的发生与发展。本综述旨在讨论CRC肠道微生物群的构成、微生物群相关致癌机制、微生物群作为CRC生物标志物的潜力,为临床应用肠道菌群治疗CRC提供新策略与新思路。     

Crohn's Disease-Associated Adherent-Invasive Escherichia coli Adhesion Is Enhanced by Exposure to the Ubiquitous Dietary Polysaccharide Maltodextrin

Crohn''s disease (CD) is associated with intestinal dysbiosis evidenced by an altered microbiome forming thick biofilms on the epithelium. Additionally, adherent-invasive E. coli (AIEC) strains are frequently isolated from ileal lesions of CD patients indicating a potential role for these strains in disease pathogenesis. The composition and characteristics of the host microbiome are influenced by environmental factors, particularly diet. Polysaccharides added to food as emulsifiers, stabilizers or bulking agents have been linked to bacteria-associated intestinal disorders. The escalating consumption of polysaccharides in Western diets parallels an increased incidence of CD during the latter 20^th century. In this study, the effect of a polysaccharide panel on adhesiveness of the CD-associated AIEC strain LF82 was analyzed to determine if these food additives promote disease-associated bacterial phenotypes. Maltodextrin (MDX), a polysaccharide derived from starch hydrolysis, markedly enhanced LF82 specific biofilm formation. Biofilm formation of multiple other E. coli strains was also promoted by MDX. MDX-induced E. coli biofilm formation was independent of polysaccharide chain length indicating a requirement for MDX metabolism. MDX exposure induced type I pili expression, which was required for MDX-enhanced biofilm formation. MDX also increased bacterial adhesion to human intestinal epithelial cell monolayers in a mechanism dependent on type 1 pili and independent of the cellular receptor CEACAM6, suggesting a novel mechanism of epithelial cell adhesion. Analysis of mucosa-associated bacteria from individuals with and without CD showed increased prevalence of malX, a gene essential for MDX metabolism, uniquely in the ileum of CD patients. These findings demonstrate that the ubiquitous dietary component MDX enhances E. coli adhesion and suggests a mechanism by which Western diets rich in specific polysaccharides may promote dysbiosis of gut microbes and contribute to disease susceptibility.