昆虫共生菌的垂直传播

共生菌普遍存在于昆虫体内,它们能够为宿主昆虫提供生长发育所必需的氨基酸、固醇类等营养物质,还能提高昆虫适应高温、寄生虫、病毒等不利环境因素的能力,昆虫则为共生菌提供稳定的生存环境和营养物质,昆虫与共生菌相互依存。多数情况下,共生菌通过垂直传播在宿主代次间进行传播,即共生菌由母代传递给子代。结合最近几年相关研究,本文综述了不同昆虫共生菌的垂直传播模式。除极少数肠道共生菌通过污染卵壳被宿主幼虫取食得以垂直传播外,垂直传播的共生菌多为经卵传播。根据侵染时期的不同,共生菌经卵传播模式多数可分为以下4种：侵染宿主昆虫幼虫中的生殖干细胞、侵染宿主昆虫年轻雌成虫中的生殖干细胞、侵染宿主昆虫雌成虫中的成熟卵母细胞以及侵染宿主昆虫囊胚期胚胎。其中,有些共生菌是以共生菌菌胞整体侵染的方式进入到宿主卵巢。另外,少数肠道共生菌也通过卵巢进行垂直传播,此类共生菌先侵染卵巢侧输卵管并在侧输卵管聚集,待卵排放至侧输卵管时再进入到卵中。在文中,我们也探讨了昆虫共生菌垂直传播过程中的细胞机制和免疫机制,包括共生菌避开宿主免疫反应、共生菌通过内吞作用进入卵巢以及不同共生菌间的协同作用等。     

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。     

LRRK2特异性调控溶菌酶的运输分泌促进肠道稳态

<正>肠道共生菌在人体健康中发挥重要作用,近年来,有关肠道菌群的研究日益成为科学家们感兴趣的焦点.宿主和肠道菌群共同作用调节肠道内环境稳态,有关这其中复杂机制的探索,是揭示在长期的共进化过程中,肠道菌与宿主如何实现"共生-互益"的关键所在,对研究肠道菌异常引起的疾病的发病机制具有重要意义.中国科学院生物物理研究所刘志华课题组发现了共生菌通过Nod2-LRRK2-Rab2a途径介导潘氏细胞中溶菌酶的分拣来促进共生关系,     

果蝇肠道共生菌对宿主作用的研究进展

肠道共生菌是动物体内的重要组成部分,在宿主的生长发育和健康等方面发挥着重要作用,近年来已成为国内外的研究热点.果蝇作为研究肠道微生物菌群功能的优秀模型,在肠道共生菌与宿主关系研究方面已取得许多重要进展.在本文中,我们首先对果蝇肠道微生物的组成和特征作了总结,然后对果蝇肠道共生菌在其生长发育、营养与代谢、行为反应、寿命以...     

微生物组学研究的“淘金时代”

人体及动物肠道中生存着数量庞大的共生微生物;这些微生物无时无刻不参与着宿主的生命活动。揭示这些共生微生物在宿主体内的变化规律、与宿主之间的依存和博弈关系等,将使人类更加全面的认知高等生物体的生命本质。本专刊从肠道微生物与疾病、肠道微生物群落结构、肠道微生物与宿主互作、肠道微生物资源和肠道微生物研究方法 5个层面展示了我国科研工作者在肠道微生物研究领域的新进展及新观点。     

肠道微生物屏障功能与病原菌毒力作用

人类肠道内存在大量共生菌,其可以抵抗病原菌入侵,对维持人体健康起重要保护作用,被称为肠道微生物屏障。肠道共生菌这种抵抗病原菌入侵保护宿主的作用称为定植抗力。一旦肠道菌群出现紊乱,定植抗力遭到破坏,机体获得感染的机率将明显升高。本综述就共生菌如何限制病原菌生长、抑制病原菌毒力以及反过来病原菌如何躲避竞争、促进菌群紊乱进行了综述。     

肠道共生微生物与健康和疾病

人体是个庞大的动态的微生物群落的天然寄居场所,人体的皮肤、口腔、消化道、呼吸道和生殖道等部位都寄生着大量的微生物.这些微生物与人体互惠互利,形成共生复合体.其中,肠道共生微生物与宿主的相关性及对宿主生理和病理状态的影响已经得到了很好的阐释.肠道共生微生物的主要功能是帮助宿主代谢,使得能量和可吸收的营养物质更好的被利用,为肠道上皮细胞提供营养,增强免疫功能,帮助寄主抵抗外来微生物的入侵.肠道菌群紊乱也是一些疾病的症状或诱发原因,比如肥胖、糖尿病和肠道炎症等.深入研究人类共生微生物与健康和疾病的关系,将为一些疾病的预防和治疗提供新的手段.     

昆虫体外共生菌研究进展

昆虫体外共生菌是指能在体外与宿主发生互利共生关系的微生物。体外共生菌虽然不如肠道微生物那样普遍存在于昆虫中,但也在宿主生长发育过程中扮演着重要的角色。昆虫体外共生菌一般寄生于昆虫体表或体内特异器官(如储菌器),在特定时期转移到植物组织中。体外共生菌产生的挥发物能作为宿主定位寄主植物的信号物质,能为宿主提供生长发育所需的营养物质,还参与了宿主体外免疫。对昆虫体外共生菌的研究,不仅能进一步揭示昆虫与微生物之间的互作关系,丰富昆虫共生菌的研究,还能从共生菌的角度探索害虫引诱剂和昆虫免疫豁免机制。本文对昆虫体外共生菌寄生方式、传播途径、对宿主的影响等研究成果进行了综述,旨在为害虫综合防控提供新思路。     

昆虫肠道防御及微生物稳态维持机制

在长期的进化过程中,昆虫形成了独特的肠道防御系统,主要由物理屏障和免疫系统共同作用来抵御外来微生物的入侵。如大部分后生动物一样,昆虫肠道上皮细胞无时无刻不与微生物接触,其种类从有益的共生菌、随食物进入的微生物到影响宿主生命的病原菌。在这样一种复杂的环境中,为了实现防御肠道病原微生物的同时又能维持共生微生物稳定的目的,宿主肠道上皮细胞必须在免疫应激和免疫耐受之间保持一种稳态平衡。Duox-ROS免疫系统和免疫缺陷(immune deficiency,Imd)信号通路作为肠道免疫反应的基本途径,必然参与调节此过程。本文从昆虫肠道防御组成、肠道免疫信号通路作用分子机制以及肠道免疫系统在肠道微生物群落稳态维持中的作用的最新研究进展进行综述。     

原麝和林麝冬夏两季粪便真菌菌群多样性

肠道微生物群对宿主健康的影响取决于饮食环境和宿主等因素.本研究通过Illumina MiSeq平台对冬、夏两季林麝和原麝粪便真菌ITS1区段进行测序,探究原麝和林麝肠道真菌菌群结构特性及季节因素对其多样性的影响.结果 表明,林麝和原麝肠道真菌组成中子囊菌门Ascomycota均为优势菌门,它们的相对丰度随物种和季节因素...     

短链脂肪酸调控骨代谢的作用及机制的研究进展

肠道菌群紊乱可导致宿主病理性骨质流失,其通过产生的代谢物从肠道扩散到体循环对骨代谢发挥重要的调控作用。短链脂肪酸（Short Chain Fatty Acids,SCFAs）是肠道细菌产生的代谢物家族中最受关注的代谢产物,近年来研究表明,SCFAs在骨代谢相关疾病的发生发展中具有重要调节作用。本文就其在骨骼系统中的作用、调节骨组织中细胞的机制及作为靶点防治骨代谢疾病骨质疏松的研究进行综述,并为此新兴且具有前景的研究领域在未来的基础研究和转化研究提供展望。     

The role of short-chain fatty acids in the interplay between diet,gut microbiota,and host energy metabolism

Short-chain fatty acids (SCFAs), the end products of fermentation of dietary fibers by the anaerobic intestinal microbiota, have been shown to exert multiple beneficial effects on mammalian energy metabolism. The mechanisms underlying these effects are the subject of intensive research and encompass the complex interplay between diet, gut microbiota, and host energy metabolism. This review summarizes the role of SCFAs in host energy metabolism, starting from the production by the gut microbiota to the uptake by the host and ending with the effects on host metabolism. There are interesting leads on the underlying molecular mechanisms, but there are also many apparently contradictory results. A coherent understanding of the multilevel network in which SCFAs exert their effects is hampered by the lack of quantitative data on actual fluxes of SCFAs and metabolic processes regulated by SCFAs. In this review we address questions that, when answered, will bring us a great step forward in elucidating the role of SCFAs in mammalian energy metabolism.     

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.     

Alterations in gut microbiota and metabolites associated with altitude-induced cardiac hypertrophy in rats during hypobaric hypoxia challenge

The gut microbiota is involved in host responses to high altitude. However, the dynamics of intestinal microecology and their association with altitude-related illness are poorly understood. Here, we used a rat model of hypobaric hypoxia challenge to mimic plateau exposure and monitored the gut microbiome, short-chain fatty acids (SCFAs), and bile acids (BAs) over 28 d. We identified weight loss, polycythemia, and pathological cardiac hypertrophy in hypoxic rats, accompanied by a large compositional shift in the gut microbiota, which is mainly driven by the bacterial families of Prevotellaceae, Porphyromonadaceae, and Streptococcaceae. The aberrant gut microbiota was characterized by increased abundance of the Parabacteroides, Alistipes, and Lactococcus genera and a larger Bacteroides to Prevotella ratio. Trans-omics analyses showed that the gut microbiome was significantly correlated with the metabolic abnormalities of SCFAs and BAs in feces, suggesting an interaction network remodeling of the microbiome-metabolome after the hypobaric hypoxia challenge. Interestingly, the transplantation of fecal microbiota significantly increased the diversity of the gut microbiota, partially inhibited the increased abundance of the Bacteroides and Alistipes genera, restored the decrease of plasma propionate, and moderately ameliorated cardiac hypertrophy in hypoxic rats. Our results provide an insight into the longitudinal changes in intestinal microecology during the hypobaric hypoxia challenge. Abnormalities in the gut microbiota and microbial metabolites contribute to the development of high-altitude heart disease in rats.

     

肠道微生物与线粒体之间的互作

肠道微生物与肠道细胞线粒体功能之间的关系十分密切。一方面,肠道微生物可直接或通过短链脂肪酸、硫化氢和一氧化氮等代谢产物间接影响与线粒体相关的能量代谢过程,调节线粒体活性氧的产生,调控线粒体甚至整个机体的免疫反应。另一方面,肠道细胞线粒体功能紊乱和基因组的遗传变异也会影响肠道微生物的组成和功能。本文主要介绍了肠道微生物和线粒体之间的互作关系的最新研究进展,为靶向作用于肠道菌群和线粒体以调节肠道健康提供理论依据。     

Gut microbiota derived metabolites in cardiovascular health and disease

Trillions of microbes inhabit the human gut, not only providing nutrients and energy to the host from the ingested food, but also producing metabolic bioactive signaling molecules to maintain health and elicit disease, such as cardiovascular disease (CVD). CVD is the leading cause of mortality worldwide. In this review, we presented gut microbiota derived metabolites involved in cardiovascular health and disease, including trimethylamine-N-oxide (TMAO), uremic toxins, short chain fatty acids (SCFAs), phytoestrogens, anthocyanins, bile acids and lipopolysaccharide. These gut microbiota derived metabolites play critical roles in maintaining a healthy cardiovascular function, and if dysregulated, potentially causally linked to CVD. A better understanding of the function and dynamics of gut microbiota derived metabolites holds great promise toward mechanistic predicative CVD biomarker discoveries and precise interventions.     

“微生物-肠-脑”轴介导的宿主食欲调节

人和动物的食欲受到中枢神经系统和外周激素的协同调控。近年来，一些研究指出肠道菌群的组成与变化通过多重途径影响宿主的食欲。肠道细菌分泌和产生的大量功能性代谢物如短链脂肪酸、次级胆汁酸和氨基酸衍生物等是其发挥调控作用的重要媒介物质。此外，肠道菌群还能够影响消化系统营养感知、肠迷走神经信号投递、肠道激素分泌等，这些也都会参与食欲和进食调节。在明确细菌调控食欲的作用机制后靶向调控和重组肠道微生物可能是改善宿主食欲的一种新策略，有助于厌食症、暴食症等相关疾病的诊治。     

The interplay between host cellular and gut microbial metabolism in NAFLD development and prevention

Metabolism regulation centred on insulin resistance is increasingly important in nonalcoholic fatty liver disease (NAFLD). This review focuses on the interactions between the host cellular and gut microbial metabolism during the development of NAFLD. The cellular metabolism of essential nutrients, such as glucose, lipids and amino acids, is reconstructed with inflammation, immune mechanisms and oxidative stress, and these alterations modify the intestinal, hepatic and systemic environments, and regulate the composition and activity of gut microbes. Microbial metabolites, such as short-chain fatty acids, secondary bile acids, protein fermentation products, choline and ethanol and bacterial toxicants, such as lipopolysaccharides, peptidoglycans and bacterial DNA, play vital roles in NAFLD. The microbe–metabolite relationship is crucial for the modulation of intestinal microbial composition and metabolic activity. The intestinal microbiota and their metabolites participate in epithelial cell metabolism via a series of cell receptors and signalling pathways and remodel the metabolism of various cells in the liver via the gut–liver axis. Microbial metabolic manipulation is a promising strategy for NAFLD prevention, but larger-sampled clinical trials are required for future application.     

Sex-dependent effects on the gut microbiota and host metabolome in type 1 diabetic mice

Sexual dimorphism exists in the onset and development of type 1 diabetes (T1D), but its potential pathological mechanism is poorly understood. In the present study, we examined sex-specific changes in the gut microbiome and host metabolome of T1D mice via 16S rRNA gene sequencing and nuclear magnetic resonance (NMR)-based metabolomics approach, and aimed to investigate potential mechanism of the gut microbiota-host metabolic interaction in the sexual dimorphism of T1D. Our results demonstrate that female mice had a greater shift in the gut microbiota than male mice during the development of T1D; however, host metabolome was more susceptible to T1D in male mice. The correlation network analysis indicates that T1D-induced host metabolic changes may be regulated by the gut microbiota in a sex-specific manner, mainly involving short-chain fatty acids (SCFAs) metabolism, energy metabolism, amino acid metabolism, and choline metabolism. Therefore, our study suggests that sex-dependent “gut microbiota-host metabolism axis” may be implicated in the sexual dimorphism of T1D, and the link between microbes and metabolites might contribute to the prevention and treatment of T1D.     

Butyrate Produced by Commensal Bacteria Potentiates Phorbol Esters Induced AP-1 Response in Human Intestinal Epithelial Cells

The human intestine is a balanced ecosystem well suited for bacterial survival, colonization and growth, which has evolved to be beneficial both for the host and the commensal bacteria. Here, we investigated the effect of bacterial metabolites produced by commensal bacteria on AP-1 signaling pathway, which has a plethora of effects on host physiology. Using intestinal epithelial cell lines, HT-29 and Caco-2, stably transfected with AP-1-dependent luciferase reporter gene, we tested the effect of culture supernatant from 49 commensal strains. We observed that several bacteria were able to activate the AP-1 pathway and this was correlated to the amount of short chain fatty acids (SCFAs) produced. Besides being a major source of energy for epithelial cells, SCFAs have been shown to regulate several signaling pathways in these cells. We show that propionate and butyrate are potent activators of the AP-1 pathway, butyrate being the more efficient of the two. We also observed a strong synergistic activation of AP-1 pathway when using butyrate with PMA, a PKC activator. Moreover, butyrate enhanced the PMA-induced expression of c-fos and ERK1/2 phosphorylation, but not p38 and JNK. In conclusion, we showed that SCFAs especially butyrate regulate the AP-1 signaling pathway, a feature that may contribute to the physiological impact of the gut microbiota on the host. Our results provide support for the involvement of butyrate in modulating the action of PKC in colon cancer cells.