婴幼儿肠道菌群的影响因素及其在肠道免疫中的作用

婴幼儿肠道菌群自定植起,随着年龄增长,需历经多次改变才能最终形成微生物稳态。本文主要介绍婴幼儿肠道菌群受分娩阶段、喂养方法、饮食结构、生活环境、疾病因素、药物使用后发生的改变,及其在肠道免疫功能形成中发挥的重要作用。     

基于肠道菌群探讨婴幼儿湿疹的防治进展

目的 从肠道菌群角度探讨婴幼儿湿疹的防治进展,为其后续研究和临床防治提供重要依据。方法 分析近10年基础和临床研究,综述肠道菌群与湿疹的关系以及肠道微生态制剂补充对婴幼儿湿疹的防治作用。结果 婴幼儿湿疹与肠道微生态和黏膜免疫应答系统发育尚未健全,对致敏原易感有关。肠道微生态制剂补通过补充益生菌和/或益生元,调整肠道菌群结构和宿主免疫平衡,修复微生物屏障,是预防和治疗婴幼儿湿疹的重要途径。结论 婴幼儿湿疹与肠道微生态及黏膜免疫系统未发育成熟有关,补充微生态制剂是其防治重要途径。     

陕西农村母乳喂养儿肠道菌群与体格发育研究

目的 探讨陕西农村地区0～18个月婴幼儿肠道菌群与体格发育的关系.方法 采取随机抽样的方法对55名0～18个月母乳喂养的健康婴幼儿进行粪便5种菌群的定量检测与体格发育的测量,菌群检测采用细菌培养法,调查数据采用SPSS13.0软件完成统计分析.结果 调查地区婴幼儿肠道有益菌双歧杆菌和乳酸菌的构成比例较低,肠道乳酸菌与身长(r=0.379,P<0.01)、体重(r=0.296,P<0.05)显著正相关.营养优良儿肠道粪便中双歧杆菌与肠杆菌数量的比值(B/E值:6.87)显著高于营养正常儿(B/E值:1.05).结论 肠道乳酸菌及较高的定植抗力对婴幼儿的体格发育有很大的促进作用,应通过改善肠道菌群促进婴幼儿的生长发育.     

腹泻患儿肠道菌群调查分析

作者于1992年3～6月对包头市区56例5岁以下腹泻患儿肠道中的五种菌进行了定性和定量分析,并与55例健康婴幼儿的材料作了比较。两组间的五种菌经秩和检验差异均有高度显著性(P<0.001)。腹泻患儿肠道中三种厌氧菌的数量明显低于健康婴幼儿,而二种需氧菌或兼性厌氧菌的数量明显高于健康婴幼儿。结果表明,腹泻患儿的肠道菌群发生了显著失调。本文讨论了腹泻与肠道菌群变化的关系及腹泻对正常菌群的影响,并对临床治疗婴幼儿腹泻提供可行的依据。     

婴幼儿科学喂养与肠道健康

肠道健康很大程度上有赖于稳定的肠道菌群和成熟的免疫状态。膳食因素在维持肠道健康中的作用越来越受到重视。婴幼儿时期科学喂养,如母乳喂养、适时引入固体食物、增加食物多样性、培养良好的饮食习惯将有利于建立成熟稳定的肠道菌群及免疫功能,促进肠道健康。     

北京市0~36月龄婴幼儿肠道菌群特点

目的 了解0~36月龄婴幼儿肠道菌群的变化特点以及0～6月龄是否纯母乳喂养对肠道菌群定植的影响。方法 于2021年1—4月,在北京市海淀区、昌平区及通州区招募0~36月龄健康单胎婴幼儿并收集新鲜粪便,最终纳入291例婴幼儿作为研究对象,并将77例6～36月龄的婴幼儿按照目前是否仍喂养母乳分为持续母乳喂养组和已断奶组,分析0～6月龄是否纯母乳喂养对肠道菌群的影响。利用Illumina Novaseq 6000测序平台对16S rRNA V4区进行测序。结果 1)婴幼儿肠道菌群的多样性和物种组成随年龄变化,Shannon指数随月龄呈现上升趋势。在门水平上,肠道菌群主要由变形菌门(Proteobacteria)、厚壁菌门(Firmicutes)、放线菌门(Actinobacteria)及拟杆菌门(Bacteroidetes)组成,新生儿中变形菌门丰富度最高,但随着月龄增加,厚壁菌逐渐替代变形菌成为主要优势菌。2) 在6～36月龄的婴幼儿中,若6月龄之前的喂养方式均为纯母乳喂养,那么断奶之后Shannon指数和Observed-OTUs指数高于持续母乳喂养的婴幼儿(Z=-2.400, P=0.015);在6～36月龄已断奶的婴幼儿中,6月龄之前纯母乳喂养婴幼儿肠道菌群的Shannon指数高于混合喂养(Z=-2.500, 杜拉拉P=0.011)。结论 婴幼儿肠道菌群多样性及构成随月龄变化明显,并且0～6月龄是否纯母乳喂养影响婴幼儿肠道菌群的多样性。     

陕西农村母乳喂养儿肠道菌群定植抗力的研究

目的 研究陕西农村母乳喂养婴幼儿的肠道定植抗力状况.方法 采取随机抽样的方法对55名0～18个月健康婴幼儿进行粪便双歧杆菌及肠杆菌的定量检测,计算肠道双歧杆菌与肠杆菌数量的比值.菌群检测采用细菌培养法.结果 婴幼儿肠道平均双歧杆菌与肠杆菌数量的比值大于1,在10个月前基本保持平稳,在10个月～组最高接近于2,13个月后下降,但仍高于10个月前,各年龄组间肠道双歧杆菌与肠杆菌数量的比值经方差分析无显著性差异.有36.36%婴幼儿的肠道双歧杆菌与肠杆菌数量的比值小于1.结论 部分婴幼儿需要调节肠道菌群,提高其肠道菌群定植抗力,以促进婴幼儿的健康成长.     

肠道菌群与早产儿脑发育及神经认知行为关系的研究

肠道菌群是生命各个阶段健康和疾病的重要决定因素。了解肠道菌群如何塑造婴幼儿大脑结构、功能并影响神经认知行为发育是当前重要的研究前沿。作为特殊婴幼儿群体，早产儿面临脑发育异常及不良神经行为发育的风险较高。本文总结早产儿肠道菌群定植特点，探讨肠道菌群与大脑发育和神经认知行为的潜在关联，为优化早产儿神经行为发育结局，制定相关干预策略提供理论支撑。     

腹泻患儿肠道菌群调查分析

作者于1992年3～6月对包头市区56例5岁以下腹泻患儿肠道中的五种苗进行了定性和定量分析，并与55例健康婴幼儿的材料作了比较。两组间的五种苗经秩和检验差异均有高度显著性(P<0．001)。愎泻患儿肠道中三种厌氧苗的数量明显低于健康婴幼儿，而二种需氧菌或兼性厌氧菌的数量明显高于健康婴幼儿。结果表明，腹泻患儿的肠道菌群发生了显著失调。本文讨论了腹泻与肠道菌群变化的关系及腹泻对正常菌群的影响，并对临床治疗婴幼儿腹泻提供可行的依据。     

婴幼儿肠道菌群初始定植的影响因素

肠道菌群与宿主的健康和疾病有极为密切的关系,多种因素可干扰肠道菌群的构成进而影响宿主的正常生理功能。本文将探讨胎龄、分娩方式、喂养方式、生长环境、抗生素应用、细菌间相互作用和微生态制剂的使用等诸多因素对婴幼儿肠道菌群初始定植的影响。     

Antibiotic-Induced Gut Microbiota Dysbiosis Damages the Intestinal Barrier,Increasing Food Allergy in Adult Mice

(1) Background: The use of antibiotics affects the composition of gut microbiota. Studies have suggested that the colonization of gut microbiota in early life is related to later food allergies. Still, the relationship between altered intestinal microbiota in adulthood and food allergies is unclear. (2) Methods: We established three mouse models to analyze gut microbiota dysbiosis’ impact on the intestinal barrier and determine whether this effect can increase the susceptibility to and severity of food allergy in later life. (3) Results: The antibiotic-induced gut microbiota dysbiosis significantly reduced Lachnospiraceae, Muribaculaceae, and Ruminococcaceae, and increased Enterococcaceae and Clostridiales. At the same time, the metabolic abundance was changed, including decreased short-chain fatty acids and tryptophan, as well as enhanced purine. This change is related to food allergies. After gut microbiota dysbiosis, we sensitized the mice. The content of specific IgE and IgG1 in mice serum was significantly increased, and the inflammatory response was enhanced. The dysbiosis of gut microbiota caused the sensitized mice to have more severe allergic symptoms, ruptured intestinal villi, and a decrease in tight junction proteins (TJs) when re-exposed to the allergen. (4) Conclusions: Antibiotic-induced gut microbiota dysbiosis increases the susceptibility and severity of food allergies. This event may be due to the increased intestinal permeability caused by decreased intestinal tight junction proteins and the increased inflammatory response.     

营养支持对肠道菌群与肠黏膜免疫的影响

肠内营养(EN)有助于保持肠黏膜的屏障功能,维护肠黏膜的结构完整性,促进肠黏膜固有免疫和获得性免疫的产生,维持肠道菌群的平衡和多样性。肠外营养(PN)能预防胃肠道功能障碍患者进一步营养不良的发生,挽救危重症患者的生命,然而PN会增加危重症患者感染并发症的发生。全肠外营养(TPN)时肠黏膜免疫受损,肠道菌群(GM)紊乱,滋养性喂养能显著改善肠黏膜的免疫功能,促进肠道内稳态的恢复。GM紊乱加重肠黏膜的炎症反应,或将进一步加重肠黏膜免疫的损害。因此,全面理解营养支持、GM与肠黏膜免疫之间的相互关系具有重要意义。     

Diet–Microbiota Interactions in Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointestinal tract. Although the precise etiology of IBD is largely unknown, it is widely thought that diet contributes to the development of IBD. Diet shapes the composition of the gut microbiota, which plays critical roles in intestinal homeostasis. In contrast, intestinal inflammation induces gut dysbiosis and may affect the use of dietary nutrients by host cells and the gut microbiota. The interaction of diet and the gut microbiota is perturbed in patients with IBD. Herein, we review the current knowledge of diet and gut microbiota interaction in intestinal homeostasis. We also discuss alterations of diet and gut microbiota interaction that influence the outcome and the nutritional treatment of IBD. Understanding the complex relationships between diet and the gut microbiota provides crucial insight into the pathogenesis of IBD and advances the development of new therapeutic approaches.     

肠道菌群与儿童神经系统疾病的研究进展

近年来,随着基因测序技术的发展,肠道菌群的研究越来越多。类似于人自身的基因,每个人的肠道菌群都是独一无二的,可比作“人类的第二指纹”。肠道菌群在人出生后3年内进展最快,而这也正好是婴幼儿大脑发育最关键的时期。随着年龄的增长,其肠道菌群或微生物组成也会发生变化。脑肠轴在大脑与肠道之间的联系有着重要的作用,而肠道菌群可通过多种途径直接或间接地影响脑肠轴进而对大脑功能产生影响。目前肠道菌群在成人的神经系统疾病研究较多,而肠道菌群与儿童神经系统疾病的研究尚较少,主要疾病包括孤独症谱系障碍、癫痫、注意力缺陷多动障碍以及青春期抑郁症等。因此,本文主要对肠道菌群与儿童神经系统疾病近年来的研究进展进行综述。     

Diet as a Modulator of Intestinal Microbiota in Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a chronic immune-driven inflammatory disease characterised by synovial inflammation, leading to progressive cartilage and bone destruction, impacting patients’ functional capacity and quality of life. Patients with RA have significant differences in gut microbiota composition when compared to controls. Intestinal dysbiosis influences the intestinal barrier strength, integrity and function, and diet is considered the main environmental factor impacting gut microbiota. Over the last few years, researchers have focused on the influence of single components of the diet in the modulation of intestinal microbiota in RA rather than whole dietary patterns. In this review, we focus on how the Mediterranean diet (MD), a whole dietary pattern, could possibly act as an adjuvant therapeutic approach, modulating intestinal microbiota and intestinal barrier function in order to improve RA-related outcomes. We also review the potential effects of particular components of the MD, such as n-3 polyunsaturated fatty acids (PUFAs), polyphenols and fibre.     

Exercise for the Diabetic Gut—Potential Health Effects and Underlying Mechanisms

It can be assumed that changes in the gut microbiota play a crucial role in the development of type 2 diabetes mellitus (T2DM). It is generally accepted that regular physical activity is beneficial for the prevention and therapy of T2DM. Therefore, this review analyzes the effects of exercise training on the gut microbiota composition and the intestinal barrier function in T2DM. The current literature shows that regular exercise can influence the gut microbiota composition and the intestinal barrier function with ameliorative effects on T2DM. In particular, increases in the number of short-chain fatty acid (SCFA)-producing bacteria and improvements in the gut barrier integrity with reduced endotoxemia seem to be key points for positive interactions between gut health and T2DM, resulting in improvements in low-grade systemic inflammation status and glycemic control. However, not all aspects are known in detail and further studies are needed to further examine the efficacy of different training programs, the role of myokines, SCFA-producing bacteria, and SCFAs in the relevant metabolic pathways. As microbial signatures differ in individuals who respond differently to exercise training programs, one scientific focus could be the development of computer-based methods for the personalized analysis of the gut microbiota in the context of a microbiota/microbiome-based training program.     

Intestinal Microbiota and Celiac Disease: Cause,Consequence or Co-Evolution?

It is widely recognized that the intestinal microbiota plays a role in the initiation and perpetuation of intestinal inflammation in numerous chronic conditions. Most studies report intestinal dysbiosis in celiac disease (CD) patients, untreated and treated with a gluten-free diet (GFD), compared to healthy controls. CD patients with gastrointestinal symptoms are also known to have a different microbiota compared to patients with dermatitis herpetiformis and controls, suggesting that the microbiota is involved in disease manifestation. Furthermore, a dysbiotic microbiota seems to be associated with persistent gastrointestinal symptoms in treated CD patients, suggesting its pathogenic implication in these particular cases. GFD per se influences gut microbiota composition, and thus constitutes an inevitable confounding factor in studies conducted in CD patients. To improve our understanding of whether intestinal dysbiosis is the cause or consequence of disease, prospective studies in healthy infants at family risk of CD are underway. These studies have revealed that the CD host genotype selects for the early colonizers of the infant’s gut, which together with environmental factors (e.g., breast-feeding, antibiotics, etc.) could influence the development of oral tolerance to gluten. Indeed, some CD genes and/or their altered expression play a role in bacterial colonization and sensing. In turn, intestinal dysbiosis could promote an abnormal response to gluten or other environmental CD-promoting factors (e.g., infections) in predisposed individuals. Here, we review the current knowledge of host-microbe interactions and how host genetics/epigenetics and environmental factors shape gut microbiota and may influence disease risk. We also summarize the current knowledge about the potential mechanisms of action of the intestinal microbiota and specific components that affect CD pathogenesis.     

The Interplay between the Gut Microbiome and the Immune System in the Context of Infectious Diseases throughout Life and the Role of Nutrition in Optimizing Treatment Strategies

Infectious diseases and infections remain a leading cause of death in low-income countries and a major risk to vulnerable groups, such as infants and the elderly. The immune system plays a crucial role in the susceptibility, persistence, and clearance of these infections. With 70–80% of immune cells being present in the gut, there is an intricate interplay between the intestinal microbiota, the intestinal epithelial layer, and the local mucosal immune system. In addition to the local mucosal immune responses in the gut, it is increasingly recognized that the gut microbiome also affects systemic immunity. Clinicians are more and more using the increased knowledge about these complex interactions between the immune system, the gut microbiome, and human pathogens. The now well-recognized impact of nutrition on the composition of the gut microbiota and the immune system elucidates the role nutrition can play in improving health. This review describes the mechanisms involved in maintaining the intricate balance between the microbiota, gut health, the local immune response, and systemic immunity, linking this to infectious diseases throughout life, and highlights the impact of nutrition in infectious disease prevention and treatment.