白介素-10与炎症性肠病

炎症性肠病(inflammatory bowel disease,IBD)是一种慢性、复发性的肠道炎症疾病,其明确病因目前仍不清楚.肠道免疫功能异常导致过量炎症因子释放损伤肠道黏膜在IBD发病中起着关键作用,应用免疫抑制剂减少炎症因子的释放也被应用于IBD的治疗.近年来利用细胞因子调节机体免疫功能以治疗IBD的研究日渐...     

白介素-27与炎症性肠病关系的研究进展

炎症性肠病是一组反复发生的慢性肠道非特异性炎症,其发病机制并不十分清楚,然而免疫调节异常被认为是该病发病的关键因素.白介素-27(interleukine-27,IL-27)是IL-12家族的新成员,主要由抗原提呈细胞产生,能够调节多种T细胞亚型的功能,并在感染及自身免疫性疾病中发挥重要的免疫调节作用.近年研究发现IL-27与炎症性肠病的发生、发展关系密切,本文就IL-27与炎症性肠病的关系作一综述.     

白介素-10与炎症性肠病

白介素 (IL) 10是一种重要的抑炎性细胞因子 ,对机体的免疫功能和炎症过程具有重要的调节活性。它在炎症性肠病 (IBD)中是一种重要的抗炎性细胞因子。此文对IL 10特性及在IBD中的治疗作用作一综述。     

调节性T细胞在炎症性肠病中的研究进展

炎症性肠病(IBD)是一种非特异性肠道炎症性疾病,其发病与自身免疫功能紊乱有关.Th1/Th2失衡是导致IBD的重要因素之一.然而,Th1/Th2理论并不能充分阐明IBD的发病机制.近几年来,越来越多的研究显示,调节性T细胞在炎症性肠病的发生发展中起重要的作用.本文就近年来调节性T细胞在炎症性肠病中作用的研究进展作一综述.     

调节性T细胞与炎症性肠病

炎症性肠病(IBD)包括溃疡性结肠炎(UC)和克罗恩病(CD),是一种病因和发病机制尚未完全明确的肠道疾病。肠黏膜免疫调节细胞和多种细胞因子参与免疫反应和炎症过程,免疫功能紊乱和免疫耐受异常是导致其发病的主要因素。此文就调节性T细胞与IBD的研究进展作一综述。     

炎症性肠病生物学活性标志物研究进展

炎症性肠病(IBD)各种生物学活性标志物近年已进行较深入的研究,正确认识这些标志物将有助于诊断IBD和判断炎症程度,本文回顾总结IBD有关各种生物学指标,并简要分析其临床意义。     

炎症性肠病生物学活性标志物研究进展

炎症性肠病（IBD）各种生物学活性标志物近年已进行较深入的研究，正确认识这些标志物将有助于诊断IBD和判断炎症程度，本回顾总结IBD有关各种生物学指标，并简要分析其临床意义。     

白介素-10与炎症性肠病

白介素(IL)-10是一种重要的抑炎性细胞因子，对机体的免疫功能和炎症过程具有重要的调节活性。它在炎症性肠病(IBD)中是一种重要的抗炎性细胞因子。此文对IL-10特性及在IBD中的治疗作用作一综述。     

炎症性肠病与细胞凋亡

细胞凋亡与胃肠道疾病以及炎症反应的关系是近年研究的新领域，炎症性肠病的发病过程中存在细胞凋亡的异常，并受到多种因素的影响，细胞凋亡是导致炎症性肠病发病过程中组织损伤和免疫紊乱的重要机制之一。     

Th细胞与炎症性肠病

Ｔ辅助细胞（Ｔｈ）是免疫应答中的主要反应细胞，在免疫调节中具有重要作用。ｈ细胞根据其分泌的细胞因子不同可分为Ｔｈ０、Ｔｈ１、Ｔｈ２、Ｔｈ３四个亚群。其中，Ｔｈ１／Ｔｈ２比例失衡在自身免疫疾病中的作用已得到证明。近年，Ｔｈ１／Ｔｈ２比例失衡在ＩＢＤ发病中的作用越来越爱到人们的重视，相信随着其研究的深入，有望为ＩＢＤ的治疗开辟崭新的途径。     

Serum interleukin-8 in inflammatory bowel disease

To investigate the relationship between serum concentrations of interleukin-8 (IL-8) and disease activity in inflammatory bowel disease, serum IL-8 concentrations were measured by enzyme-linked immunosorbent assay (ELISA) in 93 patients. Interleukin-8 levels were compared with plasma interleukin-6 (IL-6) levels in 80 of these patients. Interleukin-8 levels were also measured in ten patients with active Crohn's disease, before and after treatment with a defined formula polymeric diet. Of these patients, 70 out of 93 IL-8 concentrations were below the detection limit of the assay. Levels were higher in patients with active ulcerative colitis (median < 20 pg/mL, 75th centile value = 190) compared with inactive disease (median and 75th centile value < 20; P 0.05). Interleukin-8 concentrations correlated with a combined score for disease severity and extent (P= 0.01). Thirty-eight per cent (8/20) of patients with active Crohn's disease also had high levels of IL-8 but there was no significant difference between active and inactive disease. There was no correlation between serum IL-8 and plasma IL-6; on the contrary, very few patients had raised blood levels of both cytokines. In the diet treated group, serum IL-8 fell significantly after treatment (median = 37 pg/mL, range < 20–4615 before treatment, median < 20, range < 20–104 after treatment; P= 0.03). The results suggest that although IL-8 may be involved in the inflammatory process in inflammatory bowel disease, it is a poor marker of disease activity.     

粪便乳铁蛋白在炎症性肠病中的应用价值

乳铁蛋白(lactoferrin)是近年发现的、与铁结合的糖蛋白,主要分布表达于中性粒细胞、上皮细胞,以及各种组织和体液中,具有促进铁吸收、抗菌、免疫调节、抗感染、抗氧化、抗病毒等多种生物学功能,在许多炎症情况下其含量增加.新近的研究显示乳铁蛋白在炎症性肠病(IBD)患者肠黏膜及粪便中的含量明显高于正常对照组,不仅可以作为评价疾病活动性的指标,而且可以作为预测疾病复发、检测治疗效果、评价药物疗效等作用的指标.本文对乳铁蛋白在炎症性肠病中的作用进展作一综述,重点讨论乳铁蛋白在IBD中的作用.     

维生素D与炎症性肠病的研究进展

由于广泛的免疫调节及抗微生物作用,维生素D与自身免疫疾病的关系受到越来越多的关注.而对于炎症性肠病,尽管根本机制不明,但关于其发病已形成基本共识,即在一定环境因素下,由共生茵及其所产生致炎因子作用于免疫缺陷的个体,产生持续的免疫反应.由于维生素D对固有免疫、适应性免疫的调节作用及其作用方式,以及其可调控上皮细胞抑菌肤的产生,参与肠道微生态的平衡,有理由认为活性维生素D的产生和作用的不足可能参与了炎症性肠病的发病,同时维生素D可能是很有前景的预防和治疗炎症性肠病的药物.     

白细胞介素23与炎症性肠病

炎症性肠病(IBD)是一类病因不明的胃肠道慢性非特异性炎症,包括克罗恩病(CD)和溃疡性结肠炎(UC).促炎因子和抗炎因子的失衡被视为一个重要的病因[1].白细胞介素23(IL-23)属于前炎性因子,在IBD的发生、发展中起重要作用.此文就近年来IL-23在IBD发生、发展和治疗中的作用作一综述.     

炎症性肠病与骨代谢研究若干进展

骨质疏松(OP)是炎症性肠病(IBD)患者常见但易被忽视的并发症之一.IBD患者骨代谢异常的发病机制除了营养不良,钙、磷吸收异常,性腺功能减退之外,还与使用激素,炎症因子的异常活化等紧密相关.研究发现IBD患者骨质疏松发生率在15%左右,在老年IBD患者身上表现尤为显著,使用激素是其主要危险因子.IBD患者骨折发生率并没有原先预期的那么高.骨代谢指标对预测IBD患者BMD及骨折发生价值有限.     

New biological therapies in inflammatory bowel disease

Several biological therapies (monoclonal antibodies, designer molecules, recombinant cytokines) have been tested for clinical efficacy in inflammatory bowel disease, and some have been found to be effective. Anti-TNF-alpha (anti-tumour necrosis factor-alpha) antibody therapy is an important treatment modality in the treatment of active and fistulating Crohn's disease and should be considered in patients who fail standard medical therapies. Treatment with TNF-alpha-neutralizing antibodies is associated with immunosuppression that may lead to opportunistic infections and reactivation of tuberculosis, and patients should undergo Mantoux testing prior to treatment. Several other monoclonal antibodies, including anti-IL12 and anti-IFN-gamma, are currently in development for Crohn's disease. Other new approaches include ex vivo generation of regulatory T lymphocytes and antibodies that target and kill (subpopulations of) memory T lymphocytes.     

Advances in the genetics of inflammatory bowel disease

Research efforts in the inflammatory bowel diseases have been uniquely successful in identifying genetic linkage regions likely containing susceptibility genes for Crohn’s disease and ulcerative colitis. In two of these regions, definitive gene associations have been established, namely for the NOD2/ CARD 15 gene on chromosome 16 (IBD1) and the OCTN1/ SLC22A4-OCT/SLC22A5 genes on chromosome 5q (IBD5), both conferring increased risk for developing Crohn’s disease. Recently, significant gene associations have been reported for additional genes, including DLG5, MDR1, and TLR4 as well. The NOD2/CARD15 gene mutations are associated with ileal disease location and a modestly earlier age of onset compared with NOD2/CARD15 wild-type Crohn’s disease patients. Future progress in the genetics of inflammatory bowel disease will likely involve systematic phenotyping, including the incorporation of clinical subtypes and novel biomarkers. The ultimate goal of genetic research in inflammatory bowel disease is to identify the earliest biologic pathways that are altered, resulting in disease pathogenesis. Identification of these key pathways will potentially highlight novel therapeutic targets.     

Advances in the management of inflammatory bowel disease

Our understanding of inflammatory bowel diseases (IBD) is constantly evolving, and many new treatment options have emerged recently. This review critically examines the evidence for these new developments and aims to provide an overview for medical professionals involved in the care of patients with IBD. Proposed changes in the use of aminosalicylates, immunosuppressants and biological agents are described, and the evidence for several promising novel agents is reviewed.     

Advances in the pathogenesis of inflammatory bowel disease

Most people do not develop inflammatory bowel disease (IBD) in spite of the density of the commensal flora. In the past few years, several areas of gut mucosal immunology have emerged that will permit advances in the management of IBD at the bedside. The commensal flora is only beginning to be fully appreciated as another metabolic organ in the body. Innate immunity as it relates to the gut has complemented our understanding of the adaptive immune response. The most important susceptibility gene described for Crohn’s disease, the NOD2 gene, participates in the innate immune response to pathogens. Patients carrying NOD2 mutations have an increased adaptive immune response to commensal organisms as measured by higher titers of antimicrobial antibodies, such as anti-CBir and anti-Saccharomyces cerevisiae antibodies. Toll-like receptors expressed by antigen-presenting cells (APCs) in the gut and intestinal epithelial cells also play a role in recognition of intestinal flora. Within the APC category, dendritic cells link the innate and adaptive immune systems and shape the nature of the adaptive immune response to commensal bacteria. With respect to adaptive immunity, a new signaling pathway involving a distinct helper CD4 T-cell subset producing interleukin-17 may become a target for the treatment of chronic inflammatory diseases. This review focuses on developments likely to culminate in advances in patient care.