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1.
洪娜  于成功 《胃肠病学》2011,16(11):692-695
炎症性肠病(IBD)是一种慢性非特异性肠道炎症性疾病.其明确病因和发病机制至今仍不清楚。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。多项证据表明IBD患者存在肠道菌群紊乱。本文就肠道菌群在IBD发生中作用的研究进展作一综述。  相似文献   

2.
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)。病因至今不明,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的相互作用。目前研究较多的是肠道菌群与IBD发病的关系。肠道微生物的有害作用可见于一些IBD的动物模型。在这些动物模型中,动物在无菌的环境中不发生肠道炎症。Harper等人曾报道如果把已行回肠造口术的CD患的小肠流出物注入结肠,则诱导结肠炎症,然而将无菌的小肠超滤液注入结肠则不发生炎症。并不是所有的肠道细菌均可导致肠道炎症,一些细菌具有保护作用。这不但决定于它们分泌有毒物质的能力和细胞壁的成分(脂多糖,肽聚糖),也决定于DNA成分(尤其是CpG)。最近的一些研究表明,肠道微生态制剂包括乳酸杆菌、双歧杆菌和酵母菌对实验性结肠炎或人的IBD可以产生阻抑影响。  相似文献   

3.
肠道微生态在炎症性肠病发病中的作用   总被引:1,自引:0,他引:1  
炎症性肠病(IBD)是一类病因不明的肠道炎性疾病,主要包括溃疡性结肠炎和克罗恩病,其发病机制尚未清楚,可能涉及遗传、免疫和环境因素,其中肠道菌群所构成的肠道微生态可能扮演重要角色,已日益引起重视。本文通过对该领域的新进展作一概述,旨在加深对肠道微生态与IBD关系的认识以及探讨治疗IBD的新策略。  相似文献   

4.
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。  相似文献   

5.
炎症性肠病(inflammatory bowel diseases,IBD)是一种慢性复发性非特异性肠道疾病,其病因和发病机制尚未完全阐明.研究证实肠道菌群与肠粘膜之间异常的免疫调控在IBD的发生发展中起着决定性作用,纠正菌群失调的肠道微生态疗法对IBD的治疗有着重要的临床意义.间充质干细胞(mesenchymal s...  相似文献   

6.
益生菌对炎症性肠病的治疗作用   总被引:1,自引:0,他引:1  
周俊  台卫平  张玫 《胃肠病学》2006,11(10):633-636
炎症性肠病(IBD)主要包括溃疡性结肠炎(UC)和克岁恩病(CD),其病因和发病机制小明,IBD患者存在肠道内菌群失捌;IBD的药物治疗包括5-氨基水杨酸、糖皮质激素和免疫抑制剂,但疗效并不令人满意,且副作用较大,复发率较高。存寻求新的治疗方法时发现予IBD患者补充益生菌(probiotics),纠正肠道内菌群失调,对患者有治疗作用,但需进一步研究.  相似文献   

7.
陈迟  冉志华 《胃肠病学》2005,10(6):375-378
炎症性肠病(inflammatory bowel disease,IBD)包括克罗恩病(Crohn disease,CD)和溃疡性结肠炎(ulcerative colitis,UC),欧美较亚太地区常见,我国UC发病率较CD高,但近年来CD病例也日趋增多。IBD主要是由遗传、肠道菌群、肠道内环境不稳定、免疫反应紊乱和环境等多方面因素共同导致,但具体病因和发病机制目前尚未阐明。对IBD遗传因素雨易感基因的研究已成为热点,现就此方面进展作一综述。  相似文献   

8.
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。  相似文献   

9.
炎症性肠病(inflammatory bowel disease,IBD)是一种病因不明的慢性非特异性肠道炎症性疾病,包括溃疡性结肠炎(ulcerative colitis,UC)和克罗恩病(Crohn’s disease,CD)。许多研究显示肠道菌群的生态失调在IBD的发病中起着重要作用,而临床上相当一部分患者对常规治疗应答不佳或发生严重的不良反应,因此尝试益生菌调节肠道菌群来治疗IBD越来越受到重视。  相似文献   

10.
炎症性肠病与肠道细菌研究进展   总被引:4,自引:0,他引:4  
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.  相似文献   

11.
肠易激综合征(irritable bowel syndrome,IBS) 是一种复杂的多因素功能性疾病,其病因和发病机制尚未明确.肠道共生菌与宿主和平共处,互惠互利,这种关系破坏直接或间接参与宿主多种疾病的发生与发展.近年来,随着微生态学的发展,肠道菌群与IBS 发病的关系日益受到关注.大量研究显示,肠道细菌与IBS ...  相似文献   

12.
炎症性肠病患者肠道菌丛结构特征的指纹图谱分析   总被引:5,自引:0,他引:5  
目的建立炎症性肠病(IBD)患者和健康人肠道细菌DNA指纹图谱以分析其肠道菌丛的整体差异。方法应用肠杆菌基因间的重复共有序列(ERIC)-PCR技术建立10例IBD患者及10例正常对照者的肠道细菌DNA指纹图谱,分析IBD患者及正常对照者的肠道菌丛的整体差异。结果IBD患者及正常对照者的肠道菌丛存在整体差异,正常对照组ERIC.PCR指纹图谱电泳DNA条带多,主带位置无统一趋势;IBD组ERIC-PCR指纹图谱电泳DNA条带较少,且所有样本主带分布非常一致,均出现在约1.1kb处。结论正常人肠道细菌种类多,IBD患者少。IBD组1.1kb处主带可能为某一种肠道细菌中特有的序列,或为不同序列或几个序列的混合物。  相似文献   

13.
AIM: To study the role of intestinal flora in inflammatory bowel disease (IBD). METHODS: The spatial organization of intestinal flora was investigated in normal mice and in two models of murine colitis using fluorescence in situ hybridization. RESULTS: The murine small intestine was nearly bacteria-free. The normal colonic flora was organized in three distinct compartments (crypt, interlaced, and fecal), each with different bacterial compositions. Crypt bacteria were present in the cecum and proximal colon. The fecal compartment was composed of homogeneously mixed bacterial groups that directly contacted the colonic wall in the cecum but were separated from the proximal colonic wall by a dense interlaced layer. Beginning in the middle colon, a mucus gap of growing thickness physically separated all intestinal bacteria from contact with the epithelium. Colonic inflammation was accompanied with a depletion of bacteria within the fecal compartment, a reduced surface area in which feces had direct contact with the colonic wall, increased thickness and spread of the mucus gap, and massive increases of bacterial concentrations in the crypt and interlaced compartments. Adhesive and infiltrative bacteria were observed in inflamed colon only, with dominant Bacteroides species. CONCLUSION: The proximal and distal colons are functionally different organs with respect to the intestinal flora, representing a bioreactor and a segregation device. The highly organized structure of the colonic flora, its specific arrangement in different colonic segments, and its specialized response to inflammatory stimuli indicate that the intestinal flora is an innate part of host immunity that is under complex control.  相似文献   

14.
自发性细菌性腹膜炎(SBP)是终末期肝病的常见严重并发症,肠道微生态与SBP的发生、发展及预后密切相关,细菌易位是SBP发病的关键机制。归纳了肝硬化患者的肠道微生态特征,简述了肠道菌群在SBP发生、进展中的作用机制,为临床调整肠道微生态改善SBP提供理论基础。  相似文献   

15.
炎症性肠病(IBD)发病率逐年升高,成为消化系统常见疾病之一。目前认为肠道菌群紊乱以及细菌代谢产物改变等因素参与IBD致病过程。近年,细菌代谢产物丁酸盐因在IBD发病过程中发挥保护肠道黏膜屏障、抗炎症反应、预防IBD相关肿瘤发生等作用而备受关注。本文就丁酸盐与IBD的研究最新进展作一综述。  相似文献   

16.
肠道微生态在非酒精性脂肪性肝病发病机制中具有重要意义。系统阐释非酒精性脂肪性肝病与肠道菌群、肠道菌代谢物和肠屏障功能关系,结合中医药调节肠道微生态与治疗非酒精性脂肪性肝病关系的研究概况,提出调节肠道微生态、维持肠道稳态是中医药治疗非酒精性脂肪性肝病的重要策略。  相似文献   

17.
益生菌对炎症性肠病的治疗作用和机制   总被引:1,自引:0,他引:1  
杨明  韩真 《世界华人消化杂志》2007,15(14):1634-1638
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.  相似文献   

18.
BACKGROUNDSepsis is a common disease in intensive care units, with high morbidity and mortality. Intestinal microecology plays a vital part in the development and progression of this disease, possibly because sepsis and its treatment cause specific changes in the composition of the intestinal flora.AIMTo investigate the characteristics of intestinal flora disturbance in sepsis patients treated with antibiotics.METHODSIn this prospective comparative study, we enrolled ten patients with sepsis (sepsis group), hospitalized in the Department of Critical Care Medicine of the General Hospital, Ningxia Medical University, China (a class IIIa general hospital) from February 2017 to June 2017; ten patients without sepsis hospitalized in the same period (non-sepsis group) and ten healthy individuals (control group) were also enrolled. Fecal samples collected from the three groups were subjected to 16S rRNA gene sequencing and the intestinal flora diversity, structure, and composition were determined. Additionally, the dynamics of the intestinal flora diversity, structure, and composition in sepsis patients were investigated via 16S rRNA gene sequencing of samples collected 0 d, 3 d, and 7 d after admittance to the intensive care unit. Correlations between the serum levels of procalcitonin, endotoxin, diamine oxidase, and D-lactic acid and the intestinal flora composition of sepsis patients were also investigated.RESULTSCompared with the healthy control group, sepsis and non-sepsis patients showed reduced intestinal flora α-diversity and a distinct flora structure, with Firmicutes as the dominant phylum, and significantly decreased proportions of Bacteroidetes, as well as Prevotella and Lachnospira, among other genera. Of note, the proportion of Enterococcus was significantly increased in the intestinal tract of sepsis patients. Interestingly, the α-diversity in the sepsis group decreased gradually, from days 1 to 7 of treatment. However, pairwise comparisons showed that both the diversity and structure of the intestinal flora were not significantly different considering the three different time points studied. Curiously, the serum levels of procalcitonin, endotoxin, diamine oxidase, and D-lactic acid in sepsis patients correlated with the prevalence of various bacterial genera. For example, the prevalence of Ruminococcus was positively correlated with serum procalcitonin, endotoxins, and diamine oxidase; similarly, the prevalence of Roseburia was positively correlated with serum procalcitonin, endotoxins, and D-lactic acid.CONCLUSIONSepsis patients in intensive care units show dysbiosis, lasting for at least 1 wk.  相似文献   

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