下呼吸道微生态在支气管哮喘中的研究进展

随着二代测序的不断发展,过去人们认为无菌的下呼吸道现已被证实有多种不同的微生物群落定植.同时,越来越多的研究也证明,微生态在宿主免疫系统的发生发展中起着重要的作用.呼吸道微生态紊乱可能与多种呼吸道疾病密切相关,包括肺结核、COPD及支气管哮喘(简称哮喘)等.该研究主要回顾了近年来对哮喘患者及健康人群呼吸道微生态的研究,探讨在哮喘患者中呼吸道菌群定植的改变趋势,以及呼吸道微生态的改变与哮喘发病机制之间的关系,并且对呼吸道微生态在哮喘治疗中的研究进展进行讨论.     

呼吸道微生物组的变化及其对哮喘发病的影响

呼吸道微生物组由呼吸道菌群与其宿主细胞以及环境中影响两者相互作用的多种因素构成,如呼吸道菌群的种类、气道免疫细胞、物理化学因素等.越来越多的研究表明,呼吸道微生物组的变化与哮喘的免疫学发病存在一定的关系,对其进行深入的研究可为哮喘的诊治提供新的思路.     

寄生虫对肠道菌群和宿主免疫功能影响的研究进展

摘要：寄生虫、肠道菌群和宿主三者之间存在错综复杂的相互作用,寄生虫感染宿主后不仅可以通过分泌物或排泄物直接改变宿主的肠道菌群,还可以通过调节宿主的免疫细胞和免疫器官的功能,进一步影响宿主免疫性疾病的发生和发展。本文综述了寄生虫感染对宿主肠道菌群的物种多样性和群落结构的影响,以及寄生虫感染对宿主免疫稳态和免疫性疾病的影响,通过探讨寄生虫感染对宿主肠道菌群的作用机制,以期为调控肠道菌群靶向治疗寄生虫病提供参考。     

食用油对身体健康的影响及与肠道菌群的关系

油脂是人类饮食中重要的营养元素,它与人类生活紧密联系.长期以来人们对油脂的认识不足,造成了一些对油脂摄取的认知盲区.油脂摄入量不当会改变血中甘油三酯、胆固醇及低密度脂蛋白胆固醇浓度,增加心脑血管疾病、肥胖症、脂肪肝、胃肠道疾病等慢性病发生的危险,同时高脂饮食也会扰乱肠道微生物继而引发肠癌.目前研究发现饮食对于塑造肠道菌群至关重要,因此在无法大规模改变宿主基因组成的前提下,研究如何通过油脂影响机体疾病的发生和发展具有更现实的意义.本文从食用油摄取不当—导致菌群失调—引发各种疾病的角度来作一些简单的探讨,引导人们正确选择油脂来改善肠道菌群的平衡.     

医学蠕虫感染宿主的肠道微生物组学研究进展

寄生于哺乳动物和人类肠腔内的医学蠕虫与肠道微生物相互作用、相互调节,改变宿主肠道微环境的稳态与平衡,并影响疾病的发生、发展和预后。本文从肠道微生态、免疫反应及代谢反应等方面就医学蠕虫感染宿主治疗前后肠道微生物的研究进行综述,旨在为肠道菌群在寄生虫病的致病机制研究以及诊断治疗等方面提供新视角和理论依据。     

食物主要成分与动物肠道微生物组成及其代谢的关系

动物胃肠道中寄居有大量微生物,这些微生物的存在与宿主免疫、营养以及其他生命活动紧密相关.经过长期进化,肠道菌群与宿主形成了相对稳定的共生体系,但饮食等环境因素能够改变肠道菌群组成及其代谢活性,进而影响机体健康.另一方面,肠道菌群携带着与宿主截然不同的遗传信息,并具有比宿主更多元的代谢功能,包括从食物中摄取能量的能力,比如分解和利用不能被宿主消化的多糖.本文综述碳水化合物、蛋白质和脂类三大主要营养成分对肠道菌群及其代谢的影响,并探讨菌群变化和菌群代谢对动物健康的影响.     

肠道菌群与代谢综合征

<正>在人体的肠道内寄居着数以万亿的细菌,这些细菌组成了人体最大的微生物群,即肠道菌群。在婴儿时期影响肠道菌群结构的因素有以下几种,生产方式、婴儿喂养方式、住院接受医疗的情况(包括抗生素的使用情况)以及是否早熟[1]。从婴儿出生后肠道菌群就与宿主作为一个整体一起参与多种疾病的发生发展。宿主与肠道菌群以一种相互依赖的方式协同进化存在,宿主为肠道菌群的生长提供一个舒适的、独一无二的居住环境,肠道菌群为宿主提供一些宿主     

肠道菌群与心房颤动相关性的研究进展

肠道微生物群是一个复杂的动态生态系统,包含数万亿微生物,它们产生影响宿主健康和疾病发展的生物活性代谢物。近年来,大量研究证明,肠道菌群及其衍生代谢物影响着心血管疾病的发生发展,其中就包括心律失常,而心房颤动作为最常见的心律失常,不乏有关于其的相关研究。本综述就心房颤动与肠道菌群及其代谢物的相关性展开叙述。     

吸烟对肺癌患者呼吸道菌群的影响

<正>吸烟是肺癌发生的主要诱因之一,90%男性肺癌患者及75%~80%女性肺癌患者与吸烟有关,被动吸烟是非吸烟肺癌患者的重要危险因素[1]。烟草含有的病原体经呼吸道吸入,使呼吸道定植菌群发生改变。人类约20%恶性肿瘤由微生物引起,关于呼吸道菌群与肺癌发生的关系日益受到关注。现将吸烟对肺癌患者呼吸道菌群影响的研究进展综述如下。一、吸烟与呼吸道菌群1.烟草中存在的致病菌烟草中除存在已经证实的碳氧化物、醛类等约     

心肠对话:肠道菌群在心血管疾病中的作用

心血管疾病(CVD)是对人类健康构成极大威胁的一类疾病,其发生、发展往往受遗传与环境的多种因素影响。肠道菌群是人体内数目最大的菌群库,影响宿主的生理代谢,近年来肠道菌群与宿主间的相互作用逐渐受到重视。肠道微生物群在人类健康和疾病中发挥着重要作用,许多研究证实了肠道菌群及其代谢产物可从血脂异常、2型糖尿病、高血压、动脉粥样硬化、心力衰竭等多个方面影响CVD。因此,以肠道菌群作为CVD治疗靶点的方案值得探索。本文将对肠道菌群在CVD发病机制中的作用及通过调节肠道菌群治疗CVD的方法进行系统综述。     

Gastrointestinal Involvement in SARS-CoV-2 Infection

SARS-CoV-2 has evolved into a virus that primarily results in mild or asymptomatic disease, making its transmission more challenging to control. In addition to the respiratory tract, SARS-CoV-2 also infects the digestive tract. Some gastrointestinal symptoms occur with or before respiratory symptoms in patients with COVID-19. Respiratory infections are known to cause intestinal immune impairment and gastrointestinal symptoms. When the intestine is inflamed, cytokines affect the lung immune response and inflammation through blood circulation. The gastrointestinal microbiome may be a modifiable factor in determining the risk of SARS-CoV-2 infection and disease severity. The development of oral SARS-CoV-2 vaccine candidates and the maintenance of gut microbiota profiles may contribute to the early control of COVID-19 outbreaks. To this end, this review summarizes information on the gastrointestinal complications caused by SARS-CoV-2, SARS-CoV-2 infection, the gastrointestinal–lung axis immune response, potential control strategies for oral vaccine candidates and maintaining intestinal microbiota homeostasis.     

Influences of the Gut Microbiota on DNA Methylation and Histone Modification

The gut microbiota is a vast ensemble of microorganisms inhabiting the mammalian gastrointestinal tract that can impact physiologic and pathologic processes. However, our understanding of the underlying mechanism for the dynamic interaction between host and gut microbiota is still in its infancy. The highly evolved epigenetic modifications allow hosts to reprogram the genome in response to environmental stimuli, which may play a key role in triggering multiple human diseases. In spite of increasing studies in gut microbiota and epigenetic modifications, the correlation between them has not been well elaborated. Here, we review current knowledge of gut microbiota impacts on epigenetic modifications, the major evidence of which centers on DNA methylation and histone modification of the immune system.     

The role of the immune system in regulating the microbiota

A diverse population of bacteria, archaea, and fungi, collectively known as the microbiota, abounds within the gastrointestinal tract of the mammalian host. This microbial population makes many important contributions to host physiology through inter-kingdom signalling and by providing nutrients that have both local and systemic effects. In a healthy state the overall host-microbial interaction is symbiotic; however, a growing number of diseases have been associated with a dysregulated microbiota. To avoid these consequences, the host exerts substantial effort to maintain proper regulation of the microbiota with respect to localization and composition. Although important to maintaining microbial balance, the host immune response can also be the cause of a disrupted microbiota, contributing to disease severity. Here, we discuss the role of the host in both maintaining and disrupting a balanced gastrointestinal microbiota.     

The role of the immune system in regulating the microbiota

A diverse population of bacteria, archaea and fungi, collectively known as the microbiota, abounds within the gastrointestinal tract of the mammalian host. This microbial population makes many important contributions to host physiology through inter-kingdom signalling and by providing nutrients that have both local and systemic effects. In a healthy state the overall host-microbial interaction is symbiotic; however, a growing number of diseases have been associated with a dysregulated microbiota. To avoid these consequences, the host exerts substantial effort to maintain proper regulation of the microbiota with respect to localization and composition. Although important to maintaining microbial balance, the host immune response can also be the cause of a disrupted microbiota, contributing to disease severity. Here, we discuss the role of the host in both maintaining and disrupting a balanced gastrointestinal microbiota.     

The role of gut microbiota in immune homeostasis and autoimmunity

Keeping a delicate balance in the immune system by eliminating invading pathogens, while still maintaining self-tolerance to avoid autoimmunity, is critical for the body's health. The gut microbiota that resides in the gastrointestinal tract provides essential health benefits to its host, particularly by regulating immune homeostasis. Moreover, it has recently become obvious that alterations of these gut microbial communities can cause immune dysregulation, leading to autoimmune disorders. Here we review the advances in our understanding of how the gut microbiota regulates innate and adaptive immune homeostasis, which in turn can affect the development of not only intestinal but also systemic autoimmune diseases. Exploring the interaction of gut microbes and the host immune system will not only allow us to understand the pathogenesis of autoimmune diseases but will also provide us new foundations for the design of novel immuno- or microbe-based therapies.     

Exploring & exploiting our ‘other self’ – Does the microbiota hold the key to the future therapy in Crohn's?

Inflammatory bowel diseases (IBD) with its two major forms Crohn's disease (CD) and ulcerative colitis (UC) are chronic relapsing disorders leading to inflammation of the gastrointestinal tract. Although the precise aetiology of IBD remains unclear, several factors are believed to contribute to disease pathogenesis. Among these, the role of the intestinal microbiota has become more and more appreciated. Evidence from experimental and clinical studies strongly suggests that chronic intestinal inflammation results from a dysregulated immune response towards components of the microbiota in genetically susceptible hosts. The growing perception of the microbiota as a major driver of disease pathogenesis raises the question, if the intestinal microbiota can be used as a therapeutic target in CD. Based on what we know about host microbiota interactions in health and disease, the objective of this review is to address the question if the microbiota holds the key to the future therapy in CD.     

Neuroimmunomodulation by gut bacteria: Focus on inflammatory bowel diseases

Microbes colonize the gastrointestinal tract are considered as highest complex ecosystem because of having diverse bacterial species and 150 times more genes as compared to the human genome. Imbalance or dysbiosis in gut bacteria can cause dysregulation in gut homeostasis that subsequently activates the immune system, which leads to the development of inflammatory bowel disease(IBD). Neuromediators, including both neurotransmitters and neuropeptides, may contribute to the development of aberrant immune response. They are emerging as a regulator of inflammatory processes and play a key role in various autoimmune and inflammatory diseases. Neuromediators may influence immune cell's function via the receptors present on these cells. The cytokines secreted by the immune cells, in turn, regulate the neuronal functions by binding with their receptors present on sensory neurons. This bidirectional communication of the enteric nervous system and the enteric immune system is involved in regulating the magnitude of inflammatory pathways. Alterations in gut bacteria influence the level of neuromediators in the colon, which may affect the gastrointestinal inflammation in a disease condition. Changed neuromediators concentration via dysbiosis in gut microbiota is one of the novel approaches to understand the pathogenesis of IBD. In this article, we reviewed the existing knowledge on the role of neuromediators governing the pathogenesis of IBD, focusing on the reciprocal relationship among the gut microbiota, neuromediators, and host immunity. Understanding the neuromediators and host-microbiota interactions would give a better insight in to the disease pathophysiology and help in developing the new therapeutic approaches for the disease.     

Cytokines and respiratory syncytial virus infection

Respiratory syncytial virus (RSV) is a single-stranded negative sense RNA virus in the Paramyxovirus family that is a major cause of morbidity and life-threatening lower respiratory tract disease in infants and young children worldwide. RSV is recognized as a ubiquitous virus having considerable worldwide disease burden. Studies investigating the immune response and disease pathogenesis associated with infection attribute the interplay of the virus with host factors, particularly cytokines and chemokines, in inflammation, disease, and immune effector processes. There is convincing evidence that Th1- and Th2-type cytokine patterns determine the type of immune response to RSV infection, and that the spectrum of cytokine expression affects control mechanisms involved in the regulation of disease pathogenesis and chronicity. Thus, there is a critical need to identify virus and host mechanisms that regulate cytokine expression to allow for intervention strategies to control disease pathogenesis. In this report, we discuss the role of cytokines and chemokines in the response to RSV infection, and the potential role for suppressor of cytokine signaling (SOCS) proteins in regulating these responses.     

Glycobiome: Bacteria and mucus at the epithelial interface

The human gastrointestinal tract is colonised with a dense and diverse microbial community, that is an important player in human health and physiology. Close to the epithelial cells the mucosal microbiota is separated from the host with a thin lining of host derived glycans, including the cell surface glycocalyx and the extracellular secreted mucus. The mucosa-associated microbial composition differs from the luminal content and could be particularly important for nutrient exchange, communication with the host, development of the immune system, and resistance against invading pathogens. The mucosa-associated microbiota has adapted to the glycan rich environment by the production of mucus-degrading enzymes and mucus-binding extracellular proteins, and include mucus-degrading specialists such as Akkermansia muciniphila and Bacteroides thetaiotaomicron. This review is focussed on the host–microbe interactions within the glycan landscape at the epithelial interface and considers the spatial organisation and composition of the mucosa-associated microbiota in health and disease.