益生菌在儿童炎症性肠病中的应用

炎症性肠病（inflammatory bowel disease,IBD）是一种原因不明的慢性非特异性肠道炎性疾病,主要包括溃疡性结肠炎（ulcerative colitis,UC）、克罗恩病（Crohn's disease,CD）和未定型的炎症性肠病（IBD-unclassified,IBDU）。随着对肠道微生物与IBD关系认识的不断加深,许多研究发现肠道菌群的生态失调在IBD的发病中起着重要作用。益生菌在儿童IBD治疗中具有良好前景,但仍缺乏有效的证据来确证益生菌疗效,并指导临床对益生菌的种类和剂量等进行选择。现有研究表明,益生菌对儿童IBD的治疗具有特异性,在诱导和维持UC缓解效果明显,但在诱导CD缓解、维持CD缓解和预防术后并发症及复发方面效果并不理想。     

益生菌在炎症性肠病治疗中的研究进展

益生菌（Probiotics）是一类能够促进肠道微生物菌群平衡,对宿主健康或生理功能产生有益作用的活性微生物。目前广泛应用于生命健康领域、科学研究、生物工程、工农业以及食品安全。大量国内外研究表明益生菌在降血压、降血糖、降血脂、抗过敏、抗炎、调节免疫、维持肠道菌群平衡等方面具有积极作用。炎症性肠病的病因和发病机制尚未完全明确,现多认为与遗传、环境、感染、免疫以及肠道微生物多因素相互作用有关。益生菌通过多种机制介导,在临床治疗炎症性肠病中扮演着重要角色。     

益生菌在炎症性肠病中的治疗作用

炎症性肠病(inflammatory bowel disease,IBD)包括溃疡性结肠炎(ulcerative colitis,UC)和克罗恩病(Crohn’s disease,CD)。随着对肠道微生物群在IBD发病机制中作用的认识不断深入,近年来益生菌广泛应用于IBD治疗。大量临床试验结果表明,益生菌治疗IBD的疗效主要体现在对UC和贮袋炎的治疗,对CD的疗效不明确。益生菌治疗IBD可能通过促进肠道微生物群平衡、改善肠道屏障功能、调节肠道黏膜免疫及营养物质代谢等途径。     

细胞因子在炎症性肠病中的作用

炎症性肠病(inflammatory bowel disease,IBD)是一组病因未明的以慢性胃肠道炎症为特征的疾病,包括克罗恩病(Crohn's disease,CD)和溃疡性结肠炎(ulcerative colitis,UC)。细胞因子在IBD肠道炎症反应和黏膜免疫反应中起重要作用,目前已成为研究IBD发病机制的热点,本文就其在IBD中的作用作一综述。     

Th17细胞及相关细胞因子在炎症性肠病中的作用

<正>炎症性肠病(inflammatory bowel disease,IBD)包括溃疡性结肠炎(ulcerative colitis,UC)和克罗恩病(Crohn's disease,CD),是严重影响人类健康的慢性消化道疾病,其病因和致病机制尚未明确。越来越多研究表明,遗传易感性和环境因素在UC和CD的发病中起关键作用,可引起肠腔内细菌、抗原等物质移位至黏膜固有层,最终导致黏膜屏障功能异常[1]。     

益生菌治疗炎症性肠病的研究进展

炎症性肠病（inflammatory bowel disease,IBD）主要包括溃疡性结肠炎（ulcerative olitis,UC）和Crohn＇s病（Crohn＇s disease,CD）,近年来随着人们生活水平的提高以及饮食结构的变化,该病在我国的发病率逐年上升.目前研究认为IBD是由基因的易感性,环境因素激发和肠道免疫系统失调等多种因素交互作用引起的消化系统自身免疫性慢性炎症疾病.应用免疫抑制剂作为临床上治疗该病的主要手段已经有了很大的发展,却仍然存在着价格昂贵,毒副作用强,而且并不是对所有患者都有效等问题.长期使用抗生素则因容易引起肠道细菌耐药而导致菌群失调,往往使得IBD的病情更加复杂.临床研究表明IBD患者肠道内存在着严重的菌群失调,通过给予益生菌对局部的微生态环境进行调节,可使病情缓解.本文从炎症性肠病的病因学出发,对目前应用益生菌治疗IBD及其治疗机制的研究进展进行综述.     

肠道菌群在炎症性肠病发病中的作用

炎症性肠病(IBD)是一种非特异性肠道炎症性疾病,其病因和发病机制尚不完全明确。肠道菌群作为一个非常复杂的微生态系统,在IBD的患病机制中扮演着非常重要的角色。本研究就肠道微生态系统、肠道菌群与IBD发病的关系以及肠道菌群调控对IBD的作用的最新进展进行综述。     

粪菌移植在儿童炎症性肠病中的应用

炎症性肠病（IBD）是一种病因尚不明确的非特异性肠道炎症性疾病。越来越多的证据表明肠道菌群失调与IBD的发生发展密切相关。粪菌移植是通过各种方式将健康捐赠者的粪便菌群移植入患者消化道内,旨在重建患者肠道菌群从而达到对肠道内外疾病治疗的目的。肠道微生物稳态及失调在疾病发生发展中发挥作用,其中包括炎症性肠病（IBD）。越来越多的研究报道了FMT在IBD中的治疗作用,现主要阐述粪菌移植在儿童IBD中的应用。     

多巴胺能系统与炎症性肠病

多巴胺(dopamine,DA)是一种儿茶酚胺类的神经递质.多项研究表明多巴胺能信号通路是促进中枢神经系统和免疫系统之间平衡的关键因素,某些免疫细胞自身可以产生和释放DA.DA受体广泛表达于多种免疫细胞,DA能系统受损可能影响免疫稳态,从而影响自身免疫性疾病的发生和进展.这使得DA和炎症性肠病(inflammatory...     

SP和CGRP在炎症性肠病大鼠结肠中的表达规律

目的通过研究P物质（SP）和降钙素基因相关肽（CGRP）在炎症性肠病（IBD）大鼠结肠中的表达规律来探讨二者在IBD发生发展过程中发挥的作用。方法采用三硝基苯磺酸（TNBS）化学诱导建立IBD大鼠动物模型,应用real-time RT-PCR方法来检测SP和CGRP mRNA在模型不同时期结肠中的表达变化。结果随着炎症性肠病病理变化的加剧（第3、7天）,sP和CGRP在结肠组织中的表达水平显著升高;随着疾病的恢复（第21、28天）,其表达水平逐渐降低并趋向于正常水平。从总体来看,在IBD大鼠结肠组织中,SP和CGRP mRNA水平的变化与IBD的发生、发展呈正相关。结论神经递质SP和CGRP在IBD炎症和修复中起重要的神经免疫信号传导作用。     

炎症性肠病动物模型的研究进展

克罗恩病和溃疡性结肠炎统称为炎症性肠病（IBD）,病因虽不明确,但对其发病机理已有了较多的了解。该病的发生是由于个体易感性、肠道菌群和粘膜免疫相互作用所致。炎症性肠病动物模型可通过化学性诱导、免疫学、遗传学等方法获得。三硝基苯磺酸与乙醇灌肠致炎法是目前最常用的方法,本文侧重概述介绍三硝基苯磺酸诱导的炎症性肠病的机制、模型、应用及优缺点,为疾病的研究、治疗和新药的开发提供指导。     

Carcinoembryonic antigen (CEACAM) family members and Inflammatory Bowel Disease

Inflammatory bowel disease (IBD), encompassing Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic intestinal inflammatory condition with increasing incidence worldwide and whose pathogenesis remains largely unknown. The collected evidence indicates that genetic, environmental and microbial factors and a dysregulated immune response are responsible for the disease. IBD has an early onset and long term sufferers present a higher risk of developing colitis associated cancer (CAC). The carcinoembryonic antigen-related adhesion molecules (CEACAM) are a subgroup of the CEA family, found in a range of different cell types and organs including epithelial cells in the intestine. They can act as intercellular adhesions molecules for e.g. bacteria and soluble antigens. CEACAMs are involved in a number of different processes including cell adhesion, proliferation, differentiation and tumour suppression. Some CEACAMs such as CEACAM1, CEACAM5 and CEACAM6 are highly associated with cancer and are even recognised as valid clinical markers for certain cancer forms. However, their role in IBD pathogenesis is less understood. The purpose of this review is to provide a comprehensive summary of published literature on CEACAMs and intestinal inflammation (IBD). The interactions between CEACAMs and bacteria adhesion in relation to IBD pathophysiology will be addressed and potential new therapeutic and diagnostic opportunities will be identified.     

CD4+CD25+ 调节性T 细胞与炎症性肠病

CD4+CD25+调节性T细胞(Treg)是一种有免疫抑制功能的T淋巴细胞,其在炎症性肠病(IBD)中的功能机制已成为近年免疫学和临床研究的热点。目前,Treg细胞新的表型和作用机制逐渐被大量的实验和研究证实。本文就Treg在IBD发病过程中的作用机理及益生菌对Treg功能的影响做一综述。     

No Induction of Thiopurine Methyltransferase During Thiopurine Treatment in Inflammatory Bowel Disease

The aim of this study was to follow, during standardized initiation of thiopurine treatment, thiopurine methyltransferase (TPMT) gene expression and enzyme activity and thiopurine metabolite concentrations, and to study the role of TPMT and ITPA 94C > A polymorphisms for the development of adverse drug reactions. Sixty patients with ulcerative colitis or Crohn's disease were included in this open and prospective multi-center study. Thiopurine naïve patients were prescribed azathioprine (AZA), patients previously intolerant to AZA received 6-mercaptopurine (6-MP). The patients followed a predetermined dose escalation schedule, reaching target dose at Week 3; 2.5 and 1.25 mg/kg body weight for AZA and 6-MP, respectively. The patients were followed every week during Weeks 1–8 from baseline and then every 4 weeks until 20 weeks. TPMT activity and thiopurine metabolites were determined in erythrocytes, TPMT and ITPA genotypes, and TPMT gene expression were determined in whole blood. One homozygous TPMT-deficient patient was excluded. Five non compliant patients were withdrawn during the first weeks. Twenty-seven patients completed the study per protocol; 27 patients were withdrawn because of adverse events. Sixty-seven percent of the withdrawn patients tolerated thiopurines at a lower dose at Week 20. There was no difference in baseline TPMT enzyme activity between individuals completing the study and those withdrawn for adverse events (p = 0.45). A significant decrease in TPMT gene expression (TPMT/huCYC ratio, p = 0.02) was found, however TPMT enzyme activity did not change. TPMT heterozygous individuals had a lower probability of remaining in the study on the predetermined dose (p = 0.039). The ITPA 94C > A polymorphism was not predictive of adverse events (p = 0.35).     

多组学分析在炎症性肠病中的应用与研究进展

炎症性肠病(IBD)是一种累及回肠、直肠和结肠的特发性慢性肠道炎症性疾病,主要包括溃疡性结肠炎和克罗恩病,在临床表现、病程和治疗反应等方面具有高度异质性。目前,关于IBD的发病机制尚未明确,治疗方法相对有限。由遗传、环境、肠道微生态以及宿主免疫失衡在内的多因素共同导致了过度活跃的炎症反应并最终引发患者的肠道粘膜屏障受损和管腔菌群紊乱。单一组学的分析无法全面揭示IBD发病过程中复杂的相互协同作用机制,更无法挖掘潜在的治疗靶点和开发有效的干预策略。因此需要运用多组学关联分析技术以帮助研究者从多个维度解析IBD的发病机制。回顾和分析了多组学技术在IBD相关研究领域中的应用,并且讨论了使用这些方法在IBD分型、早期诊断和个性化医疗等领域的潜力,以期为进一步研究IBD发病机制奠定良好基础。     

白介素23 及Th17 细胞在炎症性肠病的作用

炎症性肠病(Inflammatory Bowel Diseases,IBD),是一组病因未明的累及胃肠道的慢性炎症性疾病,一般指克罗恩病(Crohn’sdisease,CD)和溃疡性结肠炎(ulcerative colitis,UC)。目前认为它是由多种因素相互作用所致的一种自身免疫性疾病,主要包括免疫、环境以及遗传等因素,其中免疫在IBD的发生过程中起着极其重要的作用。以往研究认为与T辅助细胞(T Helper cells)Th1或Th2细胞反应的增强或减弱有关。然而最近研究发现一类新细胞亚群,称为Th17细胞,与之相关的细胞因子可导致包括肠道在内的多脏器病变。Th17细胞分化过程中又需要IL-23的参与,因此IL-23/Th17细胞在炎症性肠病患者肠道内过度表达可以解释肠组织损伤的新途径,并为制定新的治疗策略提出依据。本文就IL-23/Th17轴在炎症性肠病中的作用的研究进展作一综述。     

Efficacy of Probiotics-Based Interventions as Therapy for Inflammatory Bowel Disease: A Recent Update

Probiotics such as Lactobacillus spp. play an important role in human health as they embark beneficial effect on the human gastrointestinal microflora composition and immune system. Dysbiosis in the gastrointestinal microbial composition has been identified as a major contributor to chronic inflammatory conditions, such as inflammatory bowel disease (IBD). Higher prevalence of IBD is often recorded in most of the developed Western countries, but recent data has shown an increase in previously regarded as lower risk regions, such as Japan, Malaysia, Singapore, and India. Although the IBD etiology remains a subject of speculation, the disease is likely to have developed because of interaction between extrinsic environmental elements; the host’s immune system, and the gut microbial composition. Compared to conventional treatments, probiotics and probiotic-based interventions including the introduction of specific prebiotics, symbiotic and postbiotic products had been demonstrated as more promising therapeutic measures. The present review discusses the association between gut dysbiosis, the pathogenesis of IBD, and risk factors leading to gut dysbiosis. In addition, it discusses recent studies focused on the alteration of the gastrointestinal microbiome as an effective therapy for IBD. The impact of the COVID-19 pandemic and other viral infections on IBD are also discussed in this review. Clinical and animal-based studies have shown that probiotic-based therapies can restore the gastrointestinal microbiota balance and reduce gut inflammations. Therefore, this review also assesses the status quo of these microbial-based therapies for the treatment of IBD. A better understanding of the mechanisms of their actions on modulating altered gut microbiota is required to enhance the effectiveness of the IBD therapeutics.