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。

     

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。     

肠道菌群与代谢研究进展

从出生伊始肠道菌群就依赖于宿主的基因组、营养和生活方式而变化的,与宿主共同进化发展.肠道菌群参与调控其宿主的多种代谢途径,包括宿主的免疫、营养,并且极大地影响宿主的物质能量代谢及与物质能量代谢相关疾病的发生与发展过程.同时又与多个器官共同作用,在宿主的代谢、信息传递,疾病的感染与防御方面起非常重要的作用.深入了解肠道菌群在其参与代谢的具体作用,对理解物质能量代谢相关疾病病因、优化治疗策略、调节肠道菌群、防治疾病和提高宿主健康水平具有重要作用.本研究对人类肠道菌群的形成、物质能量代谢、代谢相关疾病及其防治等方面的研究进展加以综述.     

肠道菌群及其代谢产物氧化三甲胺——冠心病治疗的新靶点

冠心病 (Coronary artery disease,CAD) 是全球发病率和死亡率最高的一种心血管疾病,冠心病和肠道菌群失调密切相关,肠道菌群可能是未来冠心病的重要诊断标志物,改善肠道菌群微环境有望成为治疗冠心病的新途径。作为肠道菌群参与合成的活性代谢产物,氧化三甲胺 (Trimethylamine-N-oxide,TMAO) 水平的升高与心血管疾病患病风险、全因死亡率的增加有关;基础研究表明TMAO可能具有促动脉粥样硬化特性;这些研究提示TMAO可作为预防和治疗冠心病的潜在靶点。文中分析了当前调控肠道菌群及其代谢产物TMAO治疗冠心病的临床及基础性研究,以期为冠心病的治疗提供帮助。     

肠道菌群及其代谢产物与结肠腺瘤性息肉相关性的研究进展

结肠癌（colorectal cancer,CRC）是常见的消化道恶性肿瘤,其发病率和病死率都极高。从结肠息肉发展到结肠癌一般需要10～15年,且大多遵循息肉‒腺瘤‒癌症的发展过程,结肠腺瘤性息肉（colorectal adenomatous polyps,CAP）被认为是结肠癌的癌前病变。有研究显示肠道菌群的改变与肠道腺瘤性息肉样变及癌症的发生发展有密切的相关性。根据肠道菌群在不同病理状态下的富集程度,可以进一步分析其与结肠病变之间的关系。本文就肠道菌群的构成,CAP患者粪便和腺瘤组织中肠道菌群富集的改变,以及肠道菌群代谢产物对CAP患者的影响等内容进行综述,为结肠腺瘤性息肉的早期诊断和治疗提供依据。     

肠道菌群与蛋白质代谢

人体的肠道内寄居着大量的微生物,在健康状态下与宿主处于共生关系,能阻止致病菌从肠道易位至人体其他部位。肠道菌群总体维持着动态平衡,并且参与宿主的新陈代谢。肠道菌群是食物消化的主要参与者,参与碳水化合物、脂肪、蛋白质、维生素等主要营养物质的分离、合成和吸收。细菌的生长需要氮源,肠道菌群通过参与机体蛋白质的代谢,一方面为自身的生长提供氮源,同时也为宿主提供必需氨基酸以满足宿主生理需求。不同类型蛋白质对菌群的作用有所不同,有些能促进菌群的生长,有些则产生抑制作用。菌源性氨基酸对宿主的健康有着重要的意义,恢复肠道内氨基酸平衡可以作为治疗诸如肠易激综合征,溃疡性结肠炎等肠道疾病的新思路。     

肠道菌群与人体代谢

人体代谢是人为了适应环境变化通过自身与微生物基因组共调节产生的所有复杂化学反应的总称。无论疾病与否,规模宏大而复杂的细菌库——肠道菌群都直接参与人体多种代谢过程。肠道菌群在人体内形成了错综复杂的微生态系统,与人类共同变化应对外界因素,人体代谢平衡状况与肠道菌群的结构组成变化密不可分。研究肠道菌群与人体代谢的相关性,对于人类健康有重要意义。     

美拉德反应产物对肠道菌群影响的研究进展

美拉德反应对肠道菌群的影响是食品营养学的研究热点之一,研究表明,美拉德反应会降低蛋白质的消化率,增加其被肠道微生物发酵利用的可能性。文章主要综述了美拉德反应产物消化和发酵特性,及其对不同疾病模型动物的肠道菌群的作用,旨在为研究美拉德反应与肠道营养健康的关系提供科学依据。     

常见肠道菌群代谢产物作为疾病诊断的指针的研究进展

人类肠道菌群能够产生多种代谢产物或与人体相互作用产生肠道菌群-宿主共代谢物,显著影响人体各大系统的生理功能。当人体健康状态以及肠道菌群发生变化时,肠道代谢物的种类和含量也会相应受到影响,因此肠道菌群代谢产物具有作为疾病诊断指针的巨大潜力。本文总结了常见的几类肠道微生物代谢产物,包括糖类、胆碱代谢物、脂质、氨基酸与肽类、维生素、胆汁酸、短链脂肪酸、酚、苯甲酰基和苯基衍生物等,及其在不同疾病状态下的作用机理,以期更好地理解肠道菌群、代谢产物和疾病之间的相关性,为疾病的预防、诊断和治疗提供新的靶点。     

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.     

病毒感染性疾病与肠道微生物关系研究进展

肠道微生物影响着人体的营养、代谢、免疫等多种生理活动,对人体健康有非常重要的影响.目前的研究表明,肠道微生物在病毒感染性疾病的感染及预后过程中发挥着重要的作用.本文分别总结了肠道病毒感染、非肠道病毒感染与肠道微生物的相互作用关系以及微生态调节干预病毒感染等内容,以期为相关研究的进一步深入和病毒感染性疾病的防治提供新思路...     

肠道菌群参与宿主免疫应答的作用及机制研究进展

肠道菌群作为动物体内重要的组成部分,能够直接参与机体的免疫调控作用,促进机体免疫系统发育,维持正常免疫功能。同时,免疫系统对肠道菌群又有调控和制约作用。本文主要综述了肠道菌群的组成以及影响肠道菌群变化的因素,系统阐述了肠道菌群与疾病相互作用的机制,总结了肠道菌群在宿主感染与免疫应答中的作用,为开展肠道菌群参与机体免疫应答的机制方面的研究提供新的思路。     

Gut feelings of safety: tolerance to the microbiota mediated by innate immune receptors

To enable microbial colonization of the gut mucosa, the intestinal immune system must not only react to danger signals but also recognize cues that indicate safety. Recognition of safety, paradoxically, is mediated by the same environmental sensors that are involved in signaling danger. Indeed, in addition to their well‐established role in inducing inflammation in response to stress signals, pattern recognition receptors and a variety of metabolic sensors also promote gut‐microbiota symbiosis by responding to “microbial symbiosis factors”, “resolution‐associated molecular patterns”, markers of energy extraction and other signals indicating the absence of pathogenic infection and tissue damage. Here we focus on how the paradoxical roles of immune receptors and other environmental sensors define the microbiota signature of an individual.     

The effector cells and cellular mediators of immune system involved in cardiac inflammation and fibrosis after myocardial infarction

The cardiac repair after myocardial infarction (MI) involves two phases, namely, inflammatory response and proliferative response. The former is an inflammatory reaction, evoked by different kinds of pro-inflammatory leukocytes and molecules stimulated by myocardial necrosis, while the latter is a repair process, predominated by a magnitude of anti-inflammatory cells and cytokines, as well as fibroblasts. Cardiac remodeling post-MI is dependent on the balance of individualized intensity of the post-MI inflammation and subsequent cardiac fibrosis. During the past 30 years, enormous studies have focused on investigating immune cells and mediators involved in cardiac inflammation and fibrosis, which are two interacting processes of post-MI cardiac repair. These results contribute to revealing the mechanism of adverse cardiac remodeling after MI and alleviating the impairment of cardiac function. In this study, we will broadly discuss the role of immune cell subpopulation and the involved cytokines and chemokines during cardiac repair post-MI, particular in cardiac inflammation and fibrosis.     

蜜蜂肠道微生物群落研究进展

蜜蜂是重要的农业传粉昆虫,对全球农业及生态维护有着不可替代的作用。然而近年来美国、欧洲等地出现蜂群大量消失的迹象,给农业经济带来严重威胁。近年来人们逐渐发现蜂肠道微生物与维持宿主健康之间存在着联系,蜜蜂属(Apis)和熊蜂属(Bombus)个体都带有简单、特异的肠道菌群,并且蜂肠道菌群与人类等其他动物具有诸多相似之处,例如其通过社会性接触稳定传播的特性。本综述介绍了近年来通过体外培养、高通量测序等技术对蜂肠道微生物与宿主关系的研究,特别是其简化的菌群结构、宿主特异性,及其对蜜蜂食物消化、营养供给、病虫抵抗等方面的作用,并探讨了未来基于我国特有蜂种研究的方向,及蜜蜂作为优良的社会性动物模式体系对未来人类营养健康研究的可行性。     

Polydatin alleviates bleomycin-induced pulmonary fibrosis and alters the gut microbiota in a mouse model

To investigate the effect and mechanism of polydatin on bleomycin (BLM)-induced pulmonary fibrosis in a mouse model. The lung fibrosis model was induced by BLM. The contents of TNF-α, LPS, IL-6 and IL-1β in lung tissue, intestine and serum were detected by ELISA. Gut microbiota diversity was detected by 16S rDNA sequencing; R language was used to analyse species composition, α-diversity, β-diversity, species differences and marker species. Mice were fed drinking water mixed with four antibiotics (ampicillin, neomycin, metronidazole, vancomycin; antibiotics, ABx) to build a mouse model of ABx-induced bacterial depletion; and faecal microbiota from different groups were transplanted into BLM-treated or untreated ABx mice. The histopathological changes and collagen I and α-SMA expression were determined. Polydatin effectively reduced the degree of fibrosis in a BLM-induced pulmonary fibrosis mouse model; BLM and/or polydatin affected the abundance of the dominant gut microbiota in mice. Moreover, faecal microbiota transplantation (FMT) from polydatin-treated BLM mice effectively alleviated lung fibrosis in BLM-treated ABx mice compared with FMT from BLM mice. Polydatin can reduce fibrosis and inflammation in a BLM-induced mouse pulmonary fibrosis model. The alteration of gut microbiota by polydatin may be involved in the therapeutic effect.     

Gut microbiota alterations are distinct for primary colorectal cancer and hepatocellular carcinoma

Colorectal cancer(CRC)and hepatocellular carcinoma(HCC)are the second and third most common causes of death by cancer,respectively.The etiologies of the two cancers are either infectious insult or due to chronic use of alcohol,smoking,diet,obesity and diabetes.Patho-logical changes in the composition of the gut microbiota that lead to intestinal inflammation are a common factor for both HCC and CRC.However,the gut microbiota of the cancer patient evolves with disease pathogenesis in unique ways that are affected by etiologies and envi-ronmental factors.in this review,we examine the chan-ges that occur in the composition of the gut microbiota across the stages of the HCC and CRC.Based on the idea that the gut microblota are an additional"lifeline"and contribute to the tumor microenvironment,we can observe from previously published literature how the microbiota can cause a shift in the balance from normal→ inflammation → diminished inflammation from early to later disease stages.This pattern leads to the hypothesis that tumor survival depends on a less pro-inflammatory tumor microenvironment.The differences observed in the gut microbiota composition between different disease etiologies as well as between HCC and CRC suggest that the tumor microenvironment is unique for each case.     

Acanthopanax senticosus total flavonoids alleviate lipopolysaccharide-induced intestinal inflammation and modulate the gut microbiota in mice

Here, we study the therapeutic effect of Acanthopanax senticosus total flavonoids (ASTFs) using a mouse intestinal inflammation model. The inflammation model used in the present study was developed through lipopolysaccharide (LPS) treatment of mice. The experimental mice were divided into a control group, model group (10 mg/kg LPS), dexamethasone group (1 mg/kg DEX) and ASTF low-, medium- and high-dosage groups (200, 400 and 800 mg/kg, respectively). The morphological and structural changes in the ileum, jejunum and duodenum were observed using HE staining. The number of intestinal goblet cells (GCs) was calculated based on PAS staining. The contents of interleukin (IL)-1β, IL-6, prostaglandin E2 (PGE2) and tumor necrosis factor α (TNF-α) were determined using enzyme-linked immunosorbent assay (ELISA) and the related mRNA expression level were measured by RT-PCR. The protein expression levels of Toll-like receptor 4 (TLR4), MyD88, p65 and p-p65 were measured using Western blotting. In addition, the 16S rRNA sequences of bacterial taxa were amplified and analyzed to assess changes in the intestinal microbes of LPS-induced mice and also in response to regulation by ASTF. Following intervention with ASTF, different therapeutic effects were shown according to the various dosages tested, all of which resulted in improved intestinal morphology and an increased number of intestinal GCs, while the contents of IL-1β, IL-6, PGE2 and TNF-α and the related mRNA expression level were significantly reduced. The TLR4, MyD88 and p-p65/p-65 protein expression levels were also significantly reduced. In addition, 16S rRNA sequencing results show that LPS disrupts the structure of mouse gut microbes, though we observed that normal microbial status can be restored through ASTF intervention.     

Gut microbiome composition is linked to whole grain-induced immunological improvements

The involvement of the gut microbiota in metabolic disorders, and the ability of whole grains to affect both host metabolism and gut microbial ecology, suggest that some benefits of whole grains are mediated through their effects on the gut microbiome. Nutritional studies that assess the effect of whole grains on both the gut microbiome and human physiology are needed. We conducted a randomized cross-over trial with four-week treatments in which 28 healthy humans consumed a daily dose of 60 g of whole-grain barley (WGB), brown rice (BR), or an equal mixture of the two (BR+WGB), and characterized their impact on fecal microbial ecology and blood markers of inflammation, glucose and lipid metabolism. All treatments increased microbial diversity, the Firmicutes/Bacteroidetes ratio, and the abundance of the genus Blautia in fecal samples. The inclusion of WGB enriched the genera Roseburia, Bifidobacterium and Dialister, and the species Eubacterium rectale, Roseburia faecis and Roseburia intestinalis. Whole grains, and especially the BR+WGB treatment, reduced plasma interleukin-6 (IL-6) and peak postprandial glucose. Shifts in the abundance of Eubacterium rectale were associated with changes in the glucose and insulin postprandial response. Interestingly, subjects with greater improvements in IL-6 levels harbored significantly higher proportions of Dialister and lower abundance of Coriobacteriaceae. In conclusion, this study revealed that a short-term intake of whole grains induced compositional alterations of the gut microbiota that coincided with improvements in host physiological measures related to metabolic dysfunctions in humans.