神经-免疫-内分泌网络与肠易激综合征

肠易激综合征(IBS)与神经-免疫-内分泌网络调节紊乱之间的联系尚未明确。此文分别从肠道神经控制、神经-免疫调节、神经-内分泌调节三个方面介绍该网络在IBS发病机制中的重要作用。     

肠易激综合征与神经-内分泌-免疫网络关系

肠易激综合征(irritable bowel syndrome,IBS)是最常见的功能性胃肠障碍,在亚洲国家患病率为2.9％～15.6％,与西方国家相似,影响多达20.0％的成年人[1].IBS发病机制尚未完全阐明,以往提出的内脏感觉过敏、脑肠作用、免疫等机制均难以全面解释.近年随着对IBS从单一生物模式向生物-心理-社会模式认识的转变,越来越多研究显示神经-内分泌-免疫网络调控异常在IBS发病中有重要作用,本文研究整理了相关国内外文献,从神经-内分泌-免疫网络角度探讨IBS发病机制.     

炎症性肠病相关内分泌疾病的研究进展

炎症性肠病(inflammatory bowel disease,IBD)是一种特发性肠道炎症性疾病,包括克罗恩病(Crohn's disease,CD)和溃疡性结肠炎(ulcerative colitis,UC).IBD可累及皮肤、骨骼、肌、肺、肝、胆、肾脏等多个器官或系统,而IBD相关内分泌疾病相对少见.本文主要对...     

炎症性肠病的遗传与免疫

炎症性肠病(IBD)是肠道慢性非特异性炎性疾病,包括溃疡性结肠炎(UC)和克罗恩病(CD),是常见的消化系统疾患之一.亚洲国家IBD患病率低于欧美国家,但近20年来国内发病率有明显上升趋势.     

肠易激综合征与神经免疫内分泌网络调控异常

肠易激综合征（IBS）与神经免疫内分泌网络调节之间的联系尚未明确。此文分别从神经系统异常、免疫系统异常、内分泌系统异常三个方面介绍该网络在IBS发病机制中的重要作用。     

肠神经胶质细胞与炎症性肠病

肠神经胶质细胞（EGC）是给予肠神经元支持和营养成分的细胞,具有维持肠神经系统（ENS）和上皮黏膜的完整性以及调节神经活动的功能。EGC可能在肠道炎症反应及免疫应答中起积极作用,EGC通过细胞因子和细胞受体的表达充当抗原提呈细胞的角色并与黏膜免疫相互作用。了解EGC与炎症性肠病（IBD）的关系有助于阐述IBD的病理生理基础,并对新的药理学干预的研制有重要作用。     

黏膜免疫与炎症性肠病

黏膜免疫被称之为“黑匣子”，它已成为21世纪生命科学研究领域中最受关注的课题。近年来，在黏膜免疫研究方面，基于基础医学和临床医学2个分支的共同努力，特别是对炎症性肠病(IBD)的发病机制与开发、研制新的治疗方法同步进行，更具有其独到之处。     

脑-肠轴与炎症性肠病关系的研究进展

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),是一种慢性、复发性肠道炎症性疾病.在我国,I B D发病率逐年上升.现阶段对于I B D发病机制的研究,焦点多集中于遗传易感性、免疫调节、环境、感染等方面,但其病因仍未完全明确.近期IBD神经调节机制的研究也逐渐引起学者的关注.目前,诸多研究发现脑-肠轴的心理-神经-内分泌-免疫调节在I B D的发病中起着重要的作用,探讨其他心理治疗方法可能会成为IBD重要的辅助治疗方案.本文就近年来关于脑-肠轴与IBD的研究进展进行阐述.     

神经-内分泌-免疫网络与哮喘关系研究进展

支气管哮喘（哮喘）是多种炎症细胞、多种细胞因子参与的气道慢性炎症性疾病,但其病变并不只局限于呼吸系统局部,还存在全身性的反应机制。神经、内分泌、免疫系统功能改变和它们之间的相互作用结果都会影响哮喘的发病过程。     

μ型阿片受体与炎症性肠病

μ型阿片受体(mu opioid receptor,MOR)作为G蛋白偶联受体的成员之一,在疼痛传递、炎症过程、免疫调节等多种生理及病理反应中发挥重要作用.MOR在中枢和外周都有大量表达,在胃肠道中主要分布于肠道淋巴细胞、肠肌层及黏膜下神经元中,对肠道蠕动、分泌功能都有重要作用.一些动物实验和体外实验结果表明MOR的激动剂在治疗炎症性肠病(inflammatory bowel disease,IBD)方面具有重要的潜在价值,已经成为治疗IBD的一种新靶点.本文对MOR的功能及其与IBD的潜在联系进行了综述,为深入研究治疗IBD的新途径提供理论依据.     

肠易激综合征与炎症性肠病

近年发现,炎症性肠病(IBD)患者发病早期或缓解期时常表现为肠易激综合征(IBs)症状,且IBD与IBS的临床表现具有一定的相似性。因而IBS与IBD的相关性受到广泛的重视。此文就IBS与IBD的发病机制及临床相关性予以阐述,以期为临床个体化治疗提供借鉴。     

Anemia and inflammatory bowel disease

Anemia is a most common complication of inflammatory bowel disease. A high frequency of low hemoglobin values in these patients often leads physicians to subestimate this condition, which translates into ineffective treatment. On the other hand, the complex nature of anemia-inducing mechanisms in inflammatory bowel disease frequently raises doubt about the most appropriate therapy. A correct identification of patients with anemia, and adequate therapy are the essential pillars for improved quality of life. The right use of iron supplementation, and novel parenteral iron formulations, either with or without associated erythropoietin, have revolutionized our approach of this complication in the course of inflammatory bowel disease.     

防御素与炎症性肠病

目前普遍认为炎症性肠病是在遗传背景的前提下,环境因素(如感染等)导致肠道免疫紊乱而发病.近年来.防御素(defensin)家族在先天性防御体系中的作用日益受到研究学者的重视.本文就防御素的种类、分布、基因表达调控、其抗微生物作用,以及其与炎症性肠病的关系和应用前景作一综述.     

Left-handedness and inflammatory bowel disease

Handedness has been reported to be associated with several disorders, including "immune disease." We examined the specific association between left-handedness and inflammatory bowel disease in 213 persons. We personally questioned 43 patients with Crohn's disease, 40 with ulcerative colitis, 70 control patients with various gastrointestinal disorders, and 60 hospital employees with no known immune or gastrointestinal disorder. The clinical diagnosis of each patient was rigorously established. Handedness was determined by The Oldfield Inventory. Study groups were well matched for age, sex, socioeconomic, and cultural backgrounds. The incidence of left-handedness among these groups was 9.3% for those with Crohn's disease, 15.0% among those with ulcerative colitis, 11.4% and 13.3% among the control groups, respectively. There was no excess of left-handedness, within any subgroup, when those with inflammatory bowel disease were analyzed according to sex; or disease location, duration, or overall severity. Our data do not confirm the previously suggested association of left-handedness and inflammatory bowel disease.     

Bacteria and inflammatory bowel disease

The cause of inflammatory bowel disease is unknown, but both environmental and genetic factors are implicated. This review presents evidence from recent studies involving both animal models and inflammatory bowel disease patients, which supports a role for bacteria in the aetiology and pathogenesis of Crohn's disease and ulcerative colitis.     

Smoking and inflammatory bowel disease

It is well established that smoking cigarettes is associated with Crohn's disease (CD) and that non-smoking is associated with ulcerative colitis (UC). Furthermore, there is convincing evidence that smoking cigarettes has a negative effect on the course of CD, and that smoking cigarettes may improve the disease severity or have a 'protective' effect in some patients with UC. Despite these well-described associations, the mechanism by which cigarette smoking affects CD and UC is not known. Researchers have studied the systemic effects, cellular and humoral immune effects, mucosal changes, and the intestinal permeability changes with inflammatory bowel disease (IBD) and smoking. To date, none of these studies adequately explains the observed clinical patterns. It has been assumed that nicotine is the active agent in these associations, but clinical trials of nicotine chewing gum and transdermal nicotine in UC have shown limited benefit, and have been complicated by significant side-effects. Topical delivery systems for nicotine therapy are currently under development and await future clinical trials.