肠道平滑肌动力与炎症性肠病研究进展

肠道平滑肌动力改变与炎症性肠病(IBD)的发病关系得到医学界的重视,并逐渐成为IBD发病机制研究的热点.肠道运动的异常和神经递质的失衡在IBD的发生和进展过程中起了重要作用;白细胞介素能在一定程度上反映肠道运动功能变化.因此,恢复神经递质的失衡并重建肠道动力平衡的策略在IBD治疗过程中有良好的应用前景.     

乳化剂对肠道菌群及炎症性肠病影响的研究进展

炎症性肠病(IBD)包括克罗恩病和溃疡性结肠炎,是一种病因不明的慢性非特异性肠道炎症性疾病,目前认为遗传、免疫、肠道菌群和环境等因素参与了IBD的发生发展过程,其中肠道菌群是近年研究的热点,应引起重视。近年来,饮食对肠道菌群及IBD影响方面的研究越来越多,有文献报道食品乳化剂通过对肠道菌群的影响在IBD的发生发展中起着促进或抑制作用。本文主要对近年来饮食中食品乳化剂对肠道菌群及IBD的影响进行综述。     

NLRP3炎症小体对炎症性肠病免疫机制影响的研究进展

炎症性肠病的发病与机体自身免疫内环境密切相关,而NLRP3炎症小体参与机体的固有免疫应答和T细胞免疫应答.慢性炎症阶段,典型的NLRP3炎症小体被过度激活,增加IL-1β和IL-18从固有层巨噬细胞和树突状细胞中的释放, IL-1β和IL-18的释放可诱导T细胞向致病性Th1和Th17的表型分化,从而维持炎症反应.急性期IL-1β主要以髓系细胞来源促进肠上皮细胞的愈合和修复,即NLRP3炎症小体对肠上皮细胞具有保护性的功能.而同时, NLRP3炎症小体介导的IL-1β的表达导致Th17/Treg失衡,这也与IBD的发病密切相关.可以说NLRP3作为肠内稳态的分子开关,通过IL-1β使局部免疫细胞向炎症表型转变.     

炎症性肠病的肠道菌群变化

炎症性肠病(IBD)是一种慢性非特异性肠道炎性疾病,其确切病因及发病机制至今仍不清楚。近年来肠道菌群与IBD发病的关系日益受到关注,多项证据表明IBD患者存在肠道菌群紊乱。此文就IBD患者肠道菌群变化及益生菌在IBD中治疗作用的研究进展作一综述。     

肠道抗原识别与炎症性肠病

炎症性肠病(inflammatory bowel disease,IBD)的患病率正不断上升.但其确切的病因和发病机制仍不清楚.对肠道抗原与IBD之间关系的研究为其发病机制的认识提供了新方向.本文详述了肠道抗原识别与IBD在临床表型、预后及家族遗传间的关系,为其进一步治疗IBD提供指导.     

炎症性肠病肠道微生物紊乱研究进展

炎症性肠病(inflammatory bowel disease,IBD)是一种发病原因未十分明确的慢性复发性肠道炎症性疾病,包括3种亚型:溃疡性结肠炎(ulcerative colitis,UC)、克罗恩病(Crohn's disease,CD)、未定型结肠炎(indeterminate colitis,IC)[1-2]。目前IBD的发病率越来越高,其发病机制可能与基因、环境、免疫及肠道菌群相关⑴。人体肠道中定植着大量的菌群、真菌、病毒,它们的失调在IBD的发病过程中可能起了非常重要的作用。有研究报道,IBD患者肠道菌群的多样性减少⑶,并且IBD的菌群失调持续存在,已经达到黏膜缓解的患者,肠道菌群依旧与健康人不同,处于失调状态⑷。     

肠道菌群与炎症性肠病

本文简述了肠道菌群与炎症性肠病(IBD)发病和诊治的关系,并展望未来对IBD进行肠道微生态的靶向治疗可能成为一种治疗新途径。     

肠道菌群对炎症性肠病诊断的研究进展

炎症性肠病(inflammatory bowel disease, IBD)是由免疫、遗传、环境三因素共同作用导致,由于它存在发病早期症状不典型及后期病变多样化的特点,因此在发病早期准确诊断IBD是一个难点,目前诊断依赖于内镜检查和影像学检查,但是患者缺乏依从性.肠道菌群在IBD中的特征性变化提示它可能成为一种新的生物标记物.近年来多项临床研究深入探讨肠道菌群在IBD鉴别诊断、疾病活动度、肠外表现等中的特征性变化,并建立肠道菌群诊断模型,获得了较高的敏感性和特异性,但由于该模型易受外界因素干扰,仍需进一步完善.本文拟将综述肠道菌群对IBD的诊断价值及临床意义.     

炎症性肠病与肠道菌群

炎症性肠病(IBD)包括溃疡性结肠炎(UC)和克罗恩病(CD),其特征是反复发生肠道溃疡,以腹痛、黏液脓血便为主要症状。IBD的发病机制仍不清楚,目前认为与宿主遗传易感性、黏膜免疫和肠道菌群有关。与正常人相比,IBD患者存在不同程度的菌群失调,主要表现在益生菌数量减少和条件致病菌数量增多。此文就IBD患者肠道菌群的分布和检测方法以及微生态制剂(MEA)对IBD的作用作一综述。     

益生菌对炎症性肠病的治疗作用和机制

炎症性肠病包括溃疡性结肠炎和克罗恩病.炎症性肠病患者肠道内存在茵群失调,若给患者补充正常细菌即益生菌,使肠道内菌群失调得到纠正,可使病情缓解.益生菌能改变肠道菌群比例、转化某些肠内物质、提高肠上皮的屏障功能、防止肠细菌易位以及通过调节细胞因子减轻炎症.本文对益生菌以上作用及机制作一综述.     

炎症性肠病与肠道细菌研究进展

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).其发病机制至今仍不清楚,可能的病因包括由基因决定的宿主易感性、黏膜免疫和肠道微生态环境三者的相互作用.近年来随着微生态学的发展,肠道菌群与IBD发病的关系日益受到关注.关于肠道病原微生物在IBD发病机制及其引起的一系列免疫学、微生态学、病理生理等方面的变化出现了研究和报道,同时微生态制剂在肠道免疫调节、控制炎症反应等方面的优点已有许多动物实验及临床应用证明,其中微生态制剂之一益生菌在IBD应用较普遍,本文就IBD与肠道菌群研究进展及益生菌制剂治疗IBD作一综述.     

Mucosal mast cells are pivotal elements in inflammatory bowel disease that connect the dots： Stress, intestinal hyperpermeability and inflammation

Mast cells (MC) are pivotal elements in several physiological and immunological functions of the gastro- intestinal (GI) tract. MC translate the stress signals that has been transmitted through brain gut axis into release of proinflammatory mediators that can cause stimulation of nerve endings that could affect afferent nerve terminals and change their perception, affect intestinal motility, increase intestinal hyperpermeability and, in susceptible individuals, modulate the inflammation. Thus, it is not surprising that MC are an important element in the pathogenesis of inflammatory bowel disease and non inflammatory GI disorders such as IBS and mast cell enterocolitis.     

肠黏膜屏障在炎症性肠病中作用机制的研究进展

炎症性肠病(inflammatory bowel disease,IBD)是肠道慢性非特异性炎症,黏膜屏障与IBD的关系密切.正常的肠黏膜屏障能维持肠道内菌群的稳定、防止肠道内细菌及毒素的移位以及对微生物进行适当的免疫防御反应起重要作用.而当发生IBD时存在肠黏膜屏障功能的障碍.本文就肠黏膜屏障功能在IBD中作用机制的研究进展作一综述.     

Regulation of the intestinal immune system by flavonoids and its utility in chronic inflammatory bowel disease

Flavonoids are phytochemicals which can regulate the activity of the intestinal immune system. In patients with chronic inflammatory bowel disease(IBD) there is an overexpression and imbalance of the components of the inflammatory immune reactions which are chronically activated. Suppression of inflammation can be achieved by anti-inflammatory drugs which are used in clinical medicine but these can cause serious side effects. Flavonoids can have natural immunosuppressive properties and inhibit the activation of immune cells and its effectors(chemokines, TNF-, cytokines). Phytochemicals such as flavonoids bind to the nuclear Ah(aryl hydrocarbon)-receptor thereby stimulating protective enzyme activities. As shown by clinical evidence in patients and by experimental work some flavonoids(apigenin, epigallocatechin gallate) were effective in the inhibition of inflammation. Instead of or additionally to anti-inflammatory drugs flavonoids can be used in IBD patients to treat the over-reactive immunologic system. This is accomplished by upregulation of the Ah-receptor. Flavonoids interact with toll-like receptors expressing on the surface of immune cells, then they were internalized to the cytosol and transferred into the nucleus, where they were attached to the Ah-receptor. The Ah-receptor binds to the Ah-R nuclear translocator and via Ah response element beneficial protective enzymes and cytokines are induced, leading to upregulation of the anti-inflammatory system.     

IL-27在炎症性肠病炎症肠黏膜中的表达及意义

目的:检测克罗恩病(CD)和溃疡性结肠炎(UC)肠黏膜组织中IL-27 p28 mRNATL其蛋白、IL-27受体mRNA的表达,探讨其在CD和UC中的发病意义.方法:应用反转录-聚合酶链反应(RT-PCR)和蛋白质免疫印迹(Western blot)方法检测炎症性肠病患者炎症肠黏膜组织中IL-27 p28基因及蛋白、IL-27受体基因的表达,并与健康者作对照.结果:IL-27 p28 mRNA在CD患者中的阳性率和灰度分析表达较UC患者明显增高(X2=6.64,P<0.05;t=11.01,P<0.01),IL-27受体阳性率和灰度分析在CD患者较UC患者和健康对照者明显增高(阳性率:X2=10.91,P<0.016,X2=18.84,P<0.016).IL-27蛋白阳性率和灰度分析在CD患者中表达明显高于UC患者(X2=5.24,P<0.05;t=3.37,P<0.05),并且IL-27mRNA的表达与蛋白质表达密切相关.结论:IL-27 p28及其受体的上调,可能有助于CD患者炎症发展过程.     

炎症性肠病合并贫血的研究进展

贫血是炎症性肠病(IBD)患者常见的并发症之一,会导致生活质量下降,也可增加患者的住院频率。据报道IBD并发贫血的发病率为6～74[1]。IBD患者贫血的发病机制尚未完全明了,铁摄入与丢失的负平衡、慢性病所致贫血、VitB12和叶酸缺乏、药物介导、炎症因子、溶血等众多因素均可能参与贫血的发生。过去普遍认为贫血是IBD不可避免的伴随症状,往往重视度不够,但最近的观点强调,贫血是此类患者明确的治疗内容。     

肠道干细胞与炎症性肠病的关系

炎症性肠病(IBD)包括克罗恩病(CD)和溃疡性结肠炎(UC),是一类病因和发病机制尚不十分明确的肠道慢性非特异性疾病。近年来其发病率呈上升趋势,但到目前为止还没有找到彻底治愈的方法。肠道干细胞是成体干细胞的一种,主要分布在肠道的隐窝,其在修复损伤的黏膜中发挥重要作用。本文就肠道干细胞与IBD的关系作一概述。     

Antibiotics and probiotics in treatment of inflammatory bowel disease

Many experimental and clinical observations suggest that intestinal microflora plays a potential role in the pathogenesis of inflammatory bowel disease (IBD). Manipulation of the luminal content using antibiotics or probiotics represents a potentially effective therapeutic option. The available studies do not support the use of antibiotics in ulcerative colitis (UC). Antibiotics are effective in treating septic complications of Crohn's disease (CD) but their use as a primary therapy is more controversial, although this approach is frequently and successfully adopted in clinical practice. There is evidence that probiotic therapy may be effective in the prevention and treatment of mild to moderate UC. In contrast, a lack of successful study data at present precludes the widespread use of probiotics in the treatment of CD. Both antibiotics and probiotics appear to play a beneficial role in the treatment and prevention of pouchitis and further trials are warranted to fully quantify their clinical efficacy.