炎症性肠病伴慢性肠道炎症的新治疗

肠道持续性慢性炎症是炎症性肠病（IBD）难以治愈的关键所在。造成肠道慢性炎症的核心机制是肠道血循环中淋巴细胞和血管内皮细胞的黏附和渗出。本文就主要黏附分子靶向抗黏附治疗的应用和临床地位作一简介。     

炎症性肠病实验研究的动物模型

炎症性肠病(IBD)主要包括溃疡性结肠炎(UC)和克罗恩病(CD),是一种反复发作的慢性非特异性肠道炎症性疾病,其确切的病因和发病机制至今还不清楚,治疗上也缺乏特异有效的药物[1]。因此,为研究其病因和发病机制以及开发新药物,建立理想的、类似于人类IBD的动物模型就显得非常重要。理想的IBD实验动物模型应具有如下特点:(1)肠道炎症的发生、病程、病理及病理生理学改变应与人类IBD相同或相似;(2)实验动物应具有明确的遗传背景;(3)实验动物应具有已知抗原易于诱导免疫反应的免疫学特点;(4)传统IBD治疗药物对其治疗有效;(5)实验动物在没…     

雷公藤多甙治疗实验性结肠炎的研究

炎症性肠病(IBD)是累及整个肠道的慢性非特异性炎症性疾病,其发病机制目前尚不清楚,大量实验证实许多炎症介质如细胞因子、趋化因子、粘附分子、炎性酶类等参与了IBD的发病机制,近年来一些转录调节因子在IBD中的作用亦引起重视.     

雷公藤多甙治疗实验性结肠炎的研究

炎症性肠病(IBD)是累及整个肠道的慢性非特异性炎症性疾病,其发病机制目前尚不清楚,大量实验证实许多炎症介质如细胞因子、趋化因子、粘附分子、炎性酶类等参与了IBD的发病机制,近年来一些转录调节因子在IBD中的作用亦引起重视.     

NGAL在炎症性肠病中的研究进展

炎症性肠病(IBD)是一种慢性复发性胃肠道炎症性疾病,包括克罗恩病和溃疡性结肠炎,其确切病因和发病机制至今未明确。中性粒细胞明胶酶相关脂质运载蛋白(NGAL)在调节肠道免疫、维持肠上皮屏障、协调肠道菌群构成中发挥重要的作用。此外,NGAL有助于IBD的临床检验。本文就NGAL在IBD中的研究进展作一综述。     

肠道菌群与肠道屏障互作在炎症性肠病中的作用研究进展

炎症性肠病(inflammatory bowel disease,IBD)是一种慢性非特异性肠道炎症性疾病,其发病机制复杂.IBD患者肠道菌群的组成与结构发生明显变化即肠道菌群失调.肠道屏障功能对维持人体肠道功能稳态发挥着重要调节作用.研究表明,在IBD中存在肠道屏障功能受损、肠道通透性增加.肠道菌群失调导致肠道屏障功...     

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炎症性肠病(inflammatory bowel disease,IBD)是一组病因不明的慢性非特异性肠道炎症性疾病,以溃疡性结肠炎(ulcrative colitis,UC)和克罗恩病(Crohn s disease,CD)最为常见。目前研究认为,IBD的发病机制是肠道菌群和环境因素作用于遗传易患人群,进而导致肠道自身免疫失衡所致,     

炎症性肠病分子病理机制及治疗进展

近年炎症性肠病(IBD)分子病理学机制及临床治疗方面有很大进展,IBD可能是遗传和环境因素共同作用导致肠道粘膜对肠道正常菌群免疫反应失常而引起的慢性炎症,NOD2的发现首次证实了IBD发病的遗传因素.针对免疫反应中各种炎症因子的干预治疗是近年IBD治疗进展最快的领域,抗TNF单克隆抗体(Infliximab)已成功地用于IBD治疗.肠道益生菌和基因治疗值得进一步开拓、深入研究.随着IBD分子发病机制的阐明,将会出现更多IBD治疗靶点.     

噬菌体与肠道菌群的相互作用及其在炎症性肠病中的研究进展

炎症性肠病(IBD)是一种自身炎症性疾病, 包括溃疡性结肠炎(UC)、克罗恩病(CD)和未定型结肠炎(IC)。由于炎症性肠病的早期症状并不典型, 难以早发现, 并且临床上难以治愈, 因此寻找炎症性肠病的新型治疗手段成为重点。近年来, 研究表明肠道菌群与IBD在疾病发生发展中互相影响, 例如肠道菌群失调可以加重肠道黏膜损伤, 调节肠道免疫反应, 引发肠道慢性炎症。而肠道慢性炎症又会影响肠道菌群, 加重菌群失调。因此, 治疗肠道菌群失调显得尤为重要。噬菌体因为其可以作用于肠道菌群而进入人们的视线, 由于其高效性、易获取、可以裂解细菌结构等特性, 近年来噬菌体与细菌如何相互作用、能否成为IBD新的治疗手段成为研究热点, 本文就噬菌体与肠道菌群的相互作用及其在IBD中的研究进展进行综述。     

炎症性肠病相关肠道菌群失调的机制及治疗的研究进展

炎症性肠病(IBD)是一种慢性反复发作的非特异性肠道炎症性疾病,其发病与多种因素相关。尽管IBD的病因尚不清楚,但肠道菌群被认为是IBD发病机制中的一个重要因素。肠道菌群对肠道免疫系统的发育和激活具有重要作用,而肠道菌群的变化可能诱发或加重IBD,但其中机制尚未完全明确,且研究发现,基于调节肠道菌群的方案对IBD的治疗具有一定的积极作用。本文就目前肠道菌群失调引起IBD的机制及相关治疗的研究进展作一综述。     

炎症性肠病肠壁纤维化机制研究进展

肠壁纤维化是炎症性肠病(IBD)常见的晚期并发症,其是一个慢性进展性过程,特点为细胞外基质(ECM)的过度沉积,导致肠壁增厚、肠腔狭窄。肠壁纤维化的形成机制尚不十分清楚,可能涉及慢性炎症与间质细胞(成纤维细胞、肌成纤维细胞)、上皮细胞与内皮细胞的转化(通过EMT和EndoMT)、多种细胞因子之间的相互作用等。对肠壁纤维化的细胞和分子机制的研究可为寻找新的IBD治疗方案提供思路。     

Dysfunctional LAD-1 neutrophils and colitis

Leukocyte adhesion deficiency 1 (LAD-1) is characterized by absent or dysfunctional beta2 integrin (CD18), leading to defective chemotaxis, adherence, phagocytosis, and bacterial killing. Colitis, except for rare intestinal necrotizing events, is not a well-recognized feature of this immunodeficiency. A case of nonspecific colitis clinically resembling Crohn's disease in a patient with the severe form of LAD-1 (0.5% < CD18) has been previously reported. We describe an adult patient with the moderate form of LAD-1 and chronic colitis characterized by extensive inflammation and ulceration of the right colon and terminal ileum, leading to adhesions and strictures. The chronic colitis described in this article associated with the dysfunctional neutrophils of LAD-1 represents a distinct pathology from the commonly encountered forms of inflammatory bowel disease (IBD). The existence of active IBD in the presence of dysfunctional CD18/CD11(a-b) intercellular adhesion molecules (ICAM-1) interaction is relevant to the proposed targeting of ICAM-1 for the treatment of Crohn's disease.     

白藜芦醇在炎症性肠病中的研究进展

炎症性肠病(IBD)是一类病因不明的肠道慢性非特异性炎症性疾病。白藜芦醇(RSV)是一种提取自红葡萄酒的天然多酚类化合物,其为NAD+依赖的组蛋白去乙酰化酶SIRT1激动剂,具有抗氧化、抗炎、抗肿瘤、抗纤维化等多种生物学活性。RSV在IBD中的作用主要包括抗炎和抗纤维化两个方面,本文就其在IBD中的研究进展作一综述。     

Old and New Lymphocyte Players in Inflammatory Bowel Disease

Inflammatory bowel disease (IBD), encompassing Crohn’s disease and ulcerative colitis, is a chronic intestinal inflammatory disorder characterized by diffuse accumulation of lymphocytes in the gut mucosa as a consequence of over-expression of endothelial adhesion molecules. The infiltrating lymphocytes have been identified as subsets of T cells, including T helper (Th)1 cells, Th17 cells, and regulatory T cells. The function of these lymphocyte subpopulations in the development of IBD is well-known, since they produce a number of pro-inflammatory cytokines, such as interferon-γ and interleukin-17A, which in turn activate mucosal proteases, thus leading to the development of intestinal lesions, i.e., ulcers, fistulas, abscesses, and strictures. However, the immune mechanisms underlying IBD are not yet fully understood, and knowledge about the function of newly discovered lymphocytes, including Th9 cells, innate lymphoid cells, mucosal-associated invariant T cells, and natural killer T cells, might add new pieces to the complex puzzle of IBD pathogenesis. This review summarizes the recent advances in the understanding of the role of mucosal lymphocytes in chronic intestinal inflammation and deals with the therapeutic potential of lymphocyte-targeting drugs in IBD patients.     

克罗恩病术后治疗和溃疡性结肠炎手术时机的抉择

炎症性肠病(IBD)包括克罗恩病(CD)和溃疡性结肠炎(UC),是一种肠道慢性非特异性炎症性疾病。尽管治疗IBD的药物层出不穷,但仍有部分患者需行手术治疗。CD的术后治疗和UC手术时机的选择对患者的生活质量的提高以及预后非常重要。本文就CD的术后治疗和UC手术时机的选择作一简单概述。     

TL1A及其受体与炎症性肠病的研究进展

炎症性肠病(IBD)是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(UC)和克罗恩病(CD)。肿瘤坏死因子配体相关分子1A(TL1A)属肿瘤坏死因子(TNF)超家族成员,其受体包括死亡受体3(DR3)和诱骗受体3(DcR3)。近年研究发现,IBD肠黏膜TL1A及其受体表达异常可能与本病的发生相关。本文就TL1A及其受体与IBD相关性的研究进展作一综述。     

骨髓干细胞治疗炎症性肠病的研究进展

炎症性肠病（inflammatory bowel disease,IBD）是一种侵及胃肠道的特发的炎症反应,包括溃疡性结肠炎（ulcerative colitis,UC）和克罗恩病（Crohn’s disease,CD）,在中国的发病率逐年上升,其可能与现代生活方式、基因遗传、肠道菌群的免疫耐受缺失、免疫反应激活等因素有关。目前的治疗在于控制活动性炎症和调节免疫紊乱,包括抗炎药物、激素、免疫抑制剂、生物治疗等多种治疗手段,但无一具有长期疗效且副作用颇多。而近年来干细胞再生、营养、免疫调节等方面的研究给IBD的治疗带来了新的希望。本文讨论了骨髓间充质干细胞及造血干细胞在IBD治疗中的新发现,回顾了干细胞在IBD治疗中可能的作用机制。     

炎症性肠病与免疫性肝病的研究进展

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）,是一种特发性肠道炎症性疾病.IBD临床表现复杂,除慢性非特异性肠道炎症外,还有皮肤、骨骼、肌、肺、肝、胆、肾脏等多个器官或系统的肠外表现.肝胆并发症因其与IBD愈后密切相关而受到关注.肝胆系统病变包括药物性肝损伤、胆结石、非酒精性脂肪肝等显性疾病,但是另外症状隐匿、特异性不强,且部分独立于肠道炎症外的免疫性肝病,如原发性硬化性胆管炎（primary scle-rosing cholagitis,PSC）、小胆管性PSC、原发性胆汁性肝硬化（primary biliary cirrhosis,PBC）、自身免疫性肝炎（AIH）、PSC/AIH重叠综合征以及lg4相关性胆管炎容易被忽视.本文就与IBD相关的免疫性肝病的研究进展进行综述.     

Antibody blockade of ICAM-1 and VCAM-1 ameliorates inflammation in the SAMP-1/Yit adoptive transfer model of Crohn's disease in mice.

BACKGROUND & AIMS: Integrins (alpha(4) and beta(2)) and their endothelial ligands vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) play key roles in leukocyte recruitment to areas of inflammation. ICAM-1 and VCAM-1 are expressed in inflamed intestinal tissues. This study investigates a possible causative role of adhesion molecules ICAM-1, VCAM-1, and alpha(4) integrins in mediating the inflammatory response in a murine model of Crohn's disease (CD). METHODS: CD4+ mesenteric lymph node cells from SAMP-1/Yit donor mice were adoptively transferred into major histocompatibility complex-matched severe combined immunodeficiency disease mice. Six weeks later, these mice were left untreated or treated for 3 days with monoclonal antibodies (mAbs) to ICAM-1, VCAM-1, or both, and alpha(4), or both ICAM-1 and alpha(4), dexamethasone, or nonblocking isotype control antibodies. On day 4 after treatment, tissues were investigated for expression of ICAM-1, VCAM-1, and for severity of inflammation using a semiquantitative inflammatory score. Dexamethasone treatment resolved all measures of intestinal inflammation. RESULTS: Blocking either ICAM-1, VCAM-1, or alpha(4) integrins had no significant beneficial effect. However, blocking ICAM-1 and alpha(4), or blocking ICAM-1 and VCAM-1, showed a 70% resolution of the active inflammation, but not chronic inflammation. CONCLUSIONS: These findings suggest that blocking ICAM-1 and VCAM-1 may have therapeutic benefit for the acute inflammatory component of Crohn's disease.