肠神经胶质细胞对肠上皮屏障的调节与功能紊乱疾病

肠神经胶质是肠神经系统的重要组成部分,其在胃肠道的黏膜中共同组成完整的神经调节体系.肠神经胶质细胞(enteric glial cells, EGCs)分布于肠壁的全层,并通过多条信号转导途径参与到了神经递质和神经调质对肠道功能的调节中.肠神经系统与肠道中的固有神经胶质细胞相互作用,参与上皮功能的调节.上皮细胞具有吸收和分泌的重要功能,同时参与到了肠道的屏障中.研究表明肠神经胶质不仅参与调控胃肠道的运动和上皮屏障功能,还参与形成肠神经元、肠内分泌细胞、免疫细胞和上皮细胞之间的细胞分子桥.本文主要对EGCs在肠道屏障和防御功能中的作用进展加以综述.     

肠神经系统的基础与临床研究进展

肠神经系统(enteric nervous system,ENS)对肠道运动、分泌功能以及与分泌-运动功能相适应的血液供应具有独立的调节作用,即其作用可不依赖中枢神经系统的调控.但ENS功能的实现有赖于肠神经与肠道肌肉、上皮细胞结构连接上的完整性,与Cajal间质细胞、胶质细胞的广泛联系,以及与中枢神经系统的协调一致.近年来,人们对肠神经系统功能的认识不断提高,新的神经递质的发现与界定及其作用机制的阐明使我们能更全面地理解ENS的生理作用.已经认识到,ENS在肠道动力性疾病和功能性胃肠病的发病中具有重要作用,如何用基础研究的结果诠释临床问题是神经胃肠病学近年的研究热点.     

肠神经胶质细胞在肠道功能与肠道疾病中的作用

肠神经胶质细胞是肠道神经系统的重要组成成分,不仅具有营养和支持肠神经元的作用,还能参与多种肠道功能的调控.异常活化的肠神经胶质细胞还可能是炎症性肠病、感染性肠炎、结肠癌等肠道疾病的重要致病因素之一.目前,肠神经胶质细胞在消化系统疾病中所发挥的作用尚不完全清楚,本文就这一方面的研究进展进行综述.     

重视研究肠道神经系统在炎症性肠病发病中作用

炎症性肠炎(inflammatory bowel disease.IBD)是一类慢性复发性肠道炎症性疾病,其病因主要涉及遗传,免疫异常,感染,环境和精神因素等多方面,其发病机制仍不清楚.最近有多项研究表明在炎症性肠病中肠神经系统(entericnervous system,ENS)结构和功能表现异常,损害ENS可引发鼠类肠道出现腹泻,血便等肠炎的表现,均提FENS调控异常参与了的IBD发病,本文就目前炎症性肠病ENS调节异常的研究现状作简要评述.     

感染后功能性胃肠病及其发病机制

功能性胃肠病（FGIDs）是一类常见胃肠道疾病，其发病和特定症候群与多种因素相关。胃肠道感染和黏膜炎症背景作为FGIDs发病的诱因近年来备受关注。学者们将那些感染后发生的FGIDs称为感染后FGIDs（PI-FGIDs）。本文就感染与FGIDs的关系以及PI-FGIDs发病机制中的动力异常、黏膜免疫改变、肠神经系统改变等内容作一介绍。     

肠易激综合征与肠道内分泌细胞

肠易激综合征(irritable bowel syndrome,IBS)是指腹痛或腹部不适,同时伴有排便习惯异常或大便性状异常的一组功能性肠病。目前一般认为IBS缺乏形态学或实验检查异常。IBS的发病机制尚不清楚,已经提出的有肠道动力异常、内脏感觉异常、脑肠相互作用、炎症、肠道神经免疫内分泌网络调控失常等。肠道内分泌在肠道的运动、感觉、分泌等方面具有重要的作用,其在IBS发病机制中的作用也倍受关注,对两者关系的研究可追溯到20年前。本文就近年来肠道内分泌细胞与IBS可能关系的研究进行概述。     

功能性肠病研究进展

1 概述。功能性肠病(functional intestinal disorders，FID)是一组表现为肠道运动与分泌功能失调而无器质性改变的综合征的总称。近年来由于研究方法学的进展，对神经内分泌、生化介质、肌电活动及心理、情感等在该病发病中的作用的探索大大深入，特别是神经胃肠病学的发展和肠神经系统(ENS)结构、功能的深入研究，初步揭示了脑肠之间的相互作用，并在某种程度上赋予功能性肠病以器质性的涵义；细胞生物学和分子生物学的进展，逐步形成了精神改变的生化概念，有助于反过来探讨情绪改变的生化基础，并深入研究其与肠道功能变化的关系。     

肠神经胶质细胞对肠黏膜免疫细胞的影响及其在炎症性肠病发生发展中的作用

肠神经胶质细胞是肠道神经系统的重要组成成分,近年来研究发现,除了营养和支持肠神经元,肠神经胶质细胞还与肠道神经-免疫-内分泌网络中的其他成员有着错综复杂的联系,并直接参与整个肠道稳态的调节.其中,肠神经胶质细胞分泌的包括神经营养因子、神经多肽、细胞因子等神经递质是肠神经胶质细胞与肠黏膜免疫细胞联系的重要桥梁,他们与免疫细胞表面的受体特异性结合后引起免疫细胞相应的生化反应.另外,肠神经胶质细胞可能还具有抗原提呈的作用,协同抗原激活肠道免疫反应.目前,肠神经胶质细胞与肠黏膜免疫细胞的关系在炎症性肠病发生发展中的作用尚不完全清楚,本文就这一方面的研究进展进行简单阐述.     

肠易激综合征与肠黏膜异常

肠易激综合征（irritable bowel syndrome，IBS）是以腹痛或腹部不适，伴有大便性状改变和排便习惯改变为特征的功能性肠道疾病，是消化科常见的疾病之一。目前，IBS的发病机制尚不明确。肠道黏膜是机体接触外环境最大的部位，拥有丰富的神经、免疫、内分泌等感觉细胞，IBS患者肠道黏膜的变化对研究IBS的发病机制具有独特的意义。本文对近年IBS与肠黏膜异常的研究进展做一综述。     

钙敏感受体在肠神经系统中的表达

目的观察与探讨G-蛋白耦联受体(CASR)在豚鼠肠神经系统中的表达。方法以豚鼠为试验对象,先进行RT-PCR设计,然后采用Western blotting来检测豚鼠肠神经系统中CASR蛋白,并且应用间接法双重免疫荧光标记对肠神经系统整体、肠神经系统中的肌间神经丛黏膜下神经丛中的CASR分布及数量等进行测定,荧光标记物采用FITC和Cy3。结果无论是肠神经系统中的肌间神经丛还是黏膜下神经丛,不同的肠神经细胞中含有不同的神经元标记物,即均存在CASR。结论豚鼠肠神经系统存在钙敏感受体的表达,因此,关于CASR在肠神经系统中的相关研究具有重要的临床意义,可能为将来研究CASR在肠道神经系统中的功能及肠炎症中的作用奠定基础。     

Fundamentals of neurogastroenterology: basic science

The focus of neurogastroenterology in Rome II was the enteric nervous system (ENS). To avoid duplication with Rome II, only advances in ENS neurobiology after Rome II are reviewed together with stronger emphasis on interactions of the brain, spinal cord, and the gut in terms of relevance for abdominal pain and disordered gastrointestinal function. A committee with expertise in selective aspects of neurogastroenterology was invited to evaluate the literature and provide a consensus overview of the Fundamentals of Neurogastroenterology textbook as they relate to functional gastrointestinal disorders (FGIDs). This review is an abbreviated version of a fuller account that appears in the forthcoming book, Rome III. This report reviews current basic science understanding of visceral sensation and its modulation by inflammation and stress and advances in the neurophysiology of the ENS. Many of the concepts are derived from animal studies in which the physiologic mechanisms underlying visceral sensitivity and neural control of motility, secretion, and blood flow are examined. Impact of inflammation and stress in experimental models relative to FGIDs is reviewed as is human brain imaging, which provides a means for translating basic science to understanding FGID symptoms. Investigative evidence and emerging concepts implicate dysfunction in the nervous system as a significant factor underlying patient symptoms in FGIDs. Continued focus on neurogastroenterologic factors that underlie the development of symptoms will lead to mechanistic understanding that is expected to directly benefit the large contingent of patients and care-givers who deal with FGIDs.     

肠神经系统退行性变的研究进展

肠神经系统(enteric nervous system,ENS)可独立调节胃肠道感觉、分泌和运动功能,ENS退行性变可导致胃肠道功能的异常,引起一系列的临床症状,其与胃肠动力性疾病和功能性胃肠病的发病有关。本文就导致ENS退行性变的原因、肠神经元退行性变引起的功能异常及其与临床症状的关联性、可能的治疗靶点等方面的研究进展作一概述。     

重视心理社会因素在功能性胃肠病中的作用

功能性胃肠病（FGIDs）是生理、精神心理和社会因素相互作用而产生的消化系统疾病，在临床上十分常见。心理社会因素在FGIDs的发病中起重要作用，不仅影响患者的胃肠生理、症状表现和疾病行为，也影响患者的生活质量、就诊要求和医疗费用。心理治疗能改善FGIDs患者的症状和病理生理异常。心理社会因素与FGIDs的关系密切，加强对精神心理社会因素在FGIDs中作用的认识十分重要。     

The gut microbiota keeps enteric glial cells on the move; prospective roles of the gut epithelium and immune system

The enteric nervous system (ENS) coordinates the major functions of the gastrointestinal tract. Its development takes place within a constantly changing environment which, after birth, culminates in the establishment of a complex gut microbiota. How such changes affect ENS development and its subsequent function throughout life is an emerging field of study that holds great interest but which is inadequately explored thus far. In this addendum, we discuss our recent findings showing that a component of the ENS, the enteric glial cell network that resides in the gut lamina propria, develops after birth and parallels the evolution of the gut microbiota. Importantly, this network was found to be malleable throughout life by incorporating new cells that arrive from the area of the gut wall in a process of directional movement which was controlled by the lumen gut microbiota. Finally, we postulate on the roles of the intestinal epithelium and the immune system as potential intermediaries between gut microbiota and ENS responses.     

The gut microbiota keeps enteric glial cells on the move; prospective roles of the gut epithelium and immune system

The enteric nervous system (ENS) coordinates the major functions of the gastrointestinal tract. Its development takes place within a constantly changing environment which, after birth, culminates in the establishment of a complex gut microbiota. How such changes affect ENS development and its subsequent function throughout life is an emerging field of study that holds great interest but which is inadequately explored thus far. In this addendum, we discuss our recent findings showing that a component of the ENS, the enteric glial cell network that resides in the gut lamina propria, develops after birth and parallels the evolution of the gut microbiota. Importantly, this network was found to be malleable throughout life by incorporating new cells that arrive from the area of the gut wall in a process of directional movement which was controlled by the lumen gut microbiota. Finally, we postulate on the roles of the intestinal epithelium and the immune system as potential intermediaries between gut microbiota and ENS responses.     

肠壁神经丛损伤和修复因素研究进展

胃肠道壁内神经丛的主要组成部分为肌间神经丛和黏膜下神经丛。肠壁神经丛损伤可表现为神经变性、神经节细胞缺失等,导致胃肠道运动、感觉、分泌功能紊乱。本文就肠壁神经丛的损伤因素(如药物、炎症)和修复因素(如神经干细胞、神经营养因子、5-HT4受体激动剂)作一综述。     

The enteric nervous system and neurogastroenterology

Neurogastroenterology is defined as neurology of the gastrointestinal tract, liver, gallbladder and pancreas and encompasses control of digestion through the enteric nervous system (ENS), the central nervous system (CNS) and integrative centers in sympathetic ganglia. This Review provides a broad overview of the field of neurogastroenterology, with a focus on the roles of the ENS in the control of the musculature of the gastrointestinal tract and transmucosal fluid movement. Digestion is controlled through the integration of multiple signals from the ENS and CNS; neural signals also pass between distinct gut regions to coordinate digestive activity. Moreover, neural and endocrine control of digestion is closely coordinated. Interestingly, the extent to which the ENS or CNS controls digestion differs considerably along the digestive tract. The importance of the ENS is emphasized by the life-threatening effects of certain ENS neuropathies, including Hirschsprung disease and Chagas disease. Other ENS disorders, such as esophageal achalasia and gastroparesis, cause varying degrees of dysfunction. The neurons in enteric reflex pathways use a wide range of chemical messengers that signal through an even wider range of receptors. These receptors provide many actual and potential targets for modifying digestive function.     

胃肠道肥大细胞与肠神经系统的相互作用

作为胃肠道免疫系统重要成员的肥大细胞与肠神经系统(ENS)间存在复杂的相互作用,其对胃肠道正常功能的维持至关重要,并与一些疾病的发生密切相关。本文综述了肥大细胞与ENS相互作用的解剖学基础和分子生物学机制及其在胃肠道疾病病理生理学机制中的作用,为探讨相关疾病新的治疗靶点提供了线索。     

Chili Peppers,Curcumins, and Prebiotics in Gastrointestinal Health and Disease

There is growing evidence for the role of several natural products as either useful agents or adjuncts in the management of functional GI disorders (FGIDs). In this review, we examine the medical evidence for three such compounds: chili, a culinary spice; curcumin, another spice and active derivative of a root bark; and prebiotics, which are nondigestible food products. Chili may affect the pathogenesis of abdominal pain especially in functional dyspepsia and cause other symptoms. It may have a therapeutic role in FGIDs through desensitization of transient receptor potential vanilloid-1 receptor. Curcumin, the active ingredient of turmeric rhizome, has been shown in several preclinical studies and uncontrolled clinical trials as having effects on gut inflammation, gut permeability and the brain–gut axis, especially in FGIDs. Prebiotics, the non-digestible food ingredients in dietary fiber, may serve as nutrients and selectively stimulate the growth and/or activity of certain colonic bacteria. The net effect of this change on colonic microbiota may lead to the production of acidic metabolites and other compounds that help to reduce the production of toxins and suppress the growth of harmful or disease-causing enteric pathogens. Although some clinical benefit in IBS has been shown, high dose intake of prebiotics may cause more bloating from bacterial fermentation.