炎症性肠病发病机制的微生物因素

炎症性肠病(IBD)的病因和发病机制尚不明确,肠道微生物与IBD发病关系密切,IBD患者肠道菌群存在失调,有证据表明,正常人群的肠黏膜免疫系统对肠道正常菌群存在耐受,而某些具有IBD遗传易感性人群的肠黏膜免疫系统对其肠道菌群失去耐受,肠道茵群参与了 IBD的发病．肠道细菌及其产物能刺激肠黏膜免疫系统,诱发这些具有IBD遗传易感性人群肠黏膜免疫系统功能紊乱,产生异常的免疫反应．不过,探究肠道细菌与IBD发病之间的关系,尚需要进一步的临床和实验研究．     

炎症性肠病肠内营养治疗的现状与进展

营养治疗与炎症性肠病(IBD)的发病机制及治疗有密切的关系,营养支持疗法可使一部分对传统内科治疗无效患者的病情得到缓解.随着治疗的进展,越来越多的学者发现深入研究两者的关系对临床有重要的意义.此文就目前肠内营养(EN)治疗在IBD 中的应用及其进展作一综述.     

四川省黑热病流行因素的探讨

通过对黑热病流行动态分析，提示在山丘地区黑热病流行因素复杂，犬利什曼病是主要传染源。当犬利什曼病发病较低时，不一定引起人类发病，即使发病也是散在的。犬利什曼病感染率升高时，病人可随之上升，局部爆发流行。白蛉的密度与黑热病关系密切。白蛉的孳生繁殖受海拔高度的制约，海拔１２００米以下和２３００米以上，即使有白蛉，密度很低，也无病人。外来人员发病率较高。     

碱性纤维母细胞生长因子与甲状腺肿瘤及Graves病关系的研究

目的 探讨碱性纤维母细胞生长因子（bFGF）与甲状腺肿瘤及Graves病之间的关系。方法 应用肝素-琼脂糖层析法、SDS-PAGE电泳法、Western blot分析法和免疫组织化学方法对bFGF进行检测。结果 分子量为14kD的bFGF与甲状腺肿瘤的发病有关，而分子量为14kD及21kD的bFGF与Graves病的发病有关。结论 14 kD bFGF的出现与甲状腺肿瘤细胞的bFGF基因异常表达有关，而14、21 kD bFGF的出现与Graves病的发病密切相关。甲状腺肿瘤与自身免疫性甲状腺疾病有共同的基因突变。     

炎症性肠病的遗传学问题

炎症性肠病的病因及发病机制中有遗传学因素的背景。本文对与炎症性肠病遗传因素有关的流行病学、免疫学、分子遗传学、某些肠道糖蛋白结构异常等问题及炎症性肠病与HLA抗原系统的关系作一介绍。     

Th17/Treg失衡与炎症性肠病的关系

炎症性肠病(inflammatory bowel disease.IBD)的病因和发病机制尚未完全明确,肠道黏膜免疫系统异常反应所导致的炎症过程在发病中起重要作用.辅助性T细胞17(T helper 17 cells,Th17)可介导慢性炎症和自身免疫性疾病的发生,调节性T细胞(regulatory T cell,Treg)有抑制自身免疫的功能,二者存在相互转化的关系.有研究表明Th17/Treg转化平衡是维持肠道免疫稳态的重要因素,这可能是导致人类IBD的原因之一.最近研究表明TGF-β,IL-6和维甲酸(retinoic acid,RA)可能是调控二者平衡关系的重要因素.肠道菌群(intestinal flora)与IBD的发生发展关系密切,益生菌(probiotics)对IBD的治疗作用成为研究的热点.深化对Th17/Treg转化调控关系的研究是当前重要的研究课题.     

Graves病患者T细胞亚群检测的意义

近年来,许多研究均证实了Graves病（GD）发病及预后与体内的自身免疫反应有明显关系。本文对GD患者外周血T细胞亚群及其与诊断及疗效的相关关系进行探讨。对象与方法38例Graves病患者,根据典型的甲状腺机能力进症（甲亢）病史、体征、血清实验室检查及甲状腺吸碘率确诊为GD,     

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.     

细胞因子与炎症性肠病

细胞因子与炎症性肠病(IBD)的关系已逐渐受到人们的重视,据其作用可分为促炎症性细胞因子和抗炎症性细胞因子。通过对细胞因子的研究可望进一步认识IBD的发病机制,为诊断和治疗IBD开辟新的途径。     

p63在脂溢性角化病中的表达及意义

目的 研究p63蛋白在脂溢性角化病中的表达,探讨其与脂溢性角化病发病的关系.方法 采用免疫组织化学S-P法检测56例脂溢性角化病和5例正常皮肤组织中p63的表达情况,并进行统计学分析.结果 脂溢性角化病中p63蛋白表达的阳性率为91.07%,与正常皮肤组织中的表达有显著性差异(P＜0.01).结论 p63蛋白参与了脂溢性角化病的发病过程,对研究脂溢性角化病的发病机制有一定意义.     

Epidemiology, genes and inflammatory bowel diseases in childhood

There is evidence that inflammatory bowel disease is immunologically mediated and that genetic factors play an important aetiological role. The identification of disease susceptibility genes has led to significant progress in our understanding of the pathogenesis of Crohn's disease. Genes linked to Crohn's disease play critical roles in the normal function of the innate immune system, and genes linked to epithelial integrity may play a role in the pathogenesis of inflammatory bowel disease as well. However, the dynamic epidemiology of both Crohn's disease and ulcerative colitis suggests that extrinsic environmental factors acting at the population level may be involved in their pathogenesis. These environmental factors may be responsible for the rising incidence of inflammatory bowel disease.     

Novel susceptibility genes in inflammatory bowel disease

The inflammatory bowel disease, Crohn's disease and ulcerative colitis, are polygenic disorders with important environmental interactions. To date, the most widely adopted approach to identifying susceptibility genes in complex diseases has involved genome wide linkage studies followed by studies of positional candidate genes in loci of interest. This review encompasses data from studies into novel candidate genes implicated in the pathogenesis of inflammatory bowel disease. Novel techniques to identify candidate genes-genome wide association studies, yeast-two hybrid screening, microarray gene expression studies and proteomic profiling, are also reviewed and their potential role in unravelling the pathogenesis of inflammatory bowel disease are discussed.     

Novel therapeutic options in the inflammatory bowel disease world

Advances in the understanding of the pathogenesis of inflammatory bowel disease have encouraged the development of many new therapies targeted at specific and non-specific mediators of the inflammatory bowel disease inflammatory pathway. The role of these therapies, including novel anti-tumour necrosis factor-alpha agents, anti-adhesion molecules, recombinant cytokines, myeloid growth factors, helminths, and probiotics, in the management of paediatric onset inflammatory bowel disease is promising and warrants further investigation.     

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.     

趋化因子及其受体在炎症性肠病中的作用

趋化因子是一类控制细胞定向迁移的细胞因子,其功能行使由趋化因子受体介导。在炎症性肠病中,许多趋化因子及其受体表达增加,并在发病机制上起着重要作用。针对趋化因子及其受体的靶向治疗能减轻炎症损伤,可望成为一种新的炎症性肠病的治疗方法。     

STAT蛋白在炎症性肠病发病机制中的作用

炎症性肠病主要包括溃疡性结肠炎和克罗恩病,是肠道慢性非特异性炎症性疾病,病因尚不十分明确,近年来认为STAT蛋白,尤其是STAT3和STAT1通过细胞因子和JAK途径在炎症性肠病的发病机制中发挥重要作用,而SOCS家族参与STAT信号通路的负向调控.     

Role of antibiotics for treatment of inflammatory bowel disease

Inflammatory bowel disease is thought to be caused by an aberrant immune response to gut bacteria in a genetically susceptible host. The gut microbiota plays an important role in the pathogenesis and complications of the two main inflammatory bowel diseases: Crohn's disease(CD) and ulcerative colitis. Alterations in gut microbiota, and specifically reduced intestinal microbial diversity, have been found to be associated with chronic gut inflammation in these disorders. Specific bacterial pathogens, such as virulent Escherichia coli strains, Bacteroides spp, and Mycobacterium avium subspecies paratuberculosis, have been linked to the pathogenesis of inflammatory bowel disease. Antibiotics may influence the course of these diseases by decreasing concentrations of bacteria in the gut lumen and altering the composition of intestinal microbiota. Different antibiotics, including ciprofloxacin, metronidazole, the combination of both, rifaximin, and anti-tuberculous regimens have been evaluated in clinical trials for the treatment of inflammatory bowel disease. For the treatment of active luminal CD, antibiotics may have a modest effect in decreasing disease activity and achieving remission, and are more effective in patients with disease involving the colon. Rifamixin, a non absorbable rifamycin has shown promising results. Treatment of suppurative complications of CD such as abscesses and fistulas, includes drainage and antibiotic therapy, most often ciprofloxacin, metronidazole, or a combination of both. Antibiotics might also play a role in maintenance of remission and prevention of post operative recurrence of CD. Data is more sparse for ulcerative colitis, and mostly consists of small trials evaluating ciprofloxacin, metronidazole and rifaximin. Most trials did not show a benefit for the treatment of active ulcerative colitis with antibiotics, though 2 meta-analyses concluded that antibiotic therapy is associated with a modest improvement in clinical symptoms. Antibiotics show a clinical benefit when used for the treatment of pouchitis. The downsides of antibiotic treatment, especially with recurrent or prolonged courses such as used in inflammatory bowel disease, are significant side effects that often cause intolerance to treatment, Clostridium dificile infection, and increasing antibiotic resistance. More studies are needed to define the exact role of antibiotics in inflammatory bowel diseases.     

人巨细胞病毒感染与炎症性肠病的相关研究进展

人巨细胞病毒(human cytomegalo virus,HCMV)是普遍存在的DNA病毒,在免疫损伤或免疫抑制的患者中常导致严重疾病.已有研究发现,HCMV在炎症性肠病(inflammatory boweldisease,IBD)的发生和发展中起一定作用.本文综述了近年来有关IBD患者中HCMV感染的临床调查和临床诊断方法,并初步探讨了HCMV感染与IBD发生的相关机制.     

The Metabolic Activity of Fecal Microbiota from Healthy Individuals and Patients with Inflammatory Bowel Disease

The hypothesis was studied that intestinal microbial metabolites play a role in the pathogenesis of inflammatory bowel disease. For that purpose, an in vitro model of the colon was inoculated with fresh feces of six healthy individuals and eight inflammatory bowel disease patients. Samples were taken from the model over time to analyze metabolites from both saccharolytic and proteolytic fermentation. Microbiotas from inflammatory bowel disease patients produced significantly more short-chain fatty acids and ammonia than microbiotas from healthy individuals. Furthermore, the branched-chain fatty acid production was 25% higher after inoculation with microbiotas from patients than after inoculation with microbiotas from healthy individuals. Phenolic compounds were produced by all microbiotas, with large interindividual variation. The production of (potentially toxic) metabolites may play a role in the onset or chronicity of inflammatory bowel disease, because they were produced in higher amounts by microbiotas from these patients than by microbiotas from healthy individuals.     

Tight junctions in inflammatory bowel diseases and inflammatory bowel disease associated colorectal cancer

Inflammatory bowel diseases are characterised by inflammation that compromises the integrity of the epithelial barrier. The intestinal epithelium is not only a static barrier but has evolved complex mechanisms to control and regulate bacterial interactions with the mucosal surface. Apical tight junction proteins are critical in the maintenance of epithelial barrier function and control of paracellular permeability. The characterisation of alterations in tight junction proteins as key players in epithelial barrier function in inflammatory bowel diseases is rapidly enhancing our understanding of critical mechanisms in disease pathogenesis as well as novel therapeutic opportunities. Here we give an overview of recent literature focusing on the role of tight junction proteins, in particular claudins, in inflammatory bowel diseases and inflammatory bowel disease associated colorectal cancer.