Diarrhea Predominant-Irritable Bowel Syndrome (IBS-D): Effects of Different Nutritional Patterns on Intestinal Dysbiosis and Symptoms

Irritable Bowel Syndrome (IBS) is a chronic functional gastrointestinal disorder characterized by abdominal pain associated with defecation or a change in bowel habits. Gut microbiota, which acts as a real organ with well-defined functions, is in a mutualistic relationship with the host, harvesting additional energy and nutrients from the diet and protecting the host from pathogens; specific alterations in its composition seem to play a crucial role in IBS pathophysiology. It is well known that diet can significantly modulate the intestinal microbiota profile but it is less known how different nutritional approach effective in IBS patients, such as the low-FODMAP diet, could be responsible of intestinal microbiota changes, thus influencing the presence of gastrointestinal (GI) symptoms. The aim of this review was to explore the effects of different nutritional protocols (e.g., traditional nutritional advice, low-FODMAP diet, gluten-free diet, etc.) on IBS-D symptoms and on intestinal microbiota variations in both IBS-D patients and healthy subjects. To date, an ideal nutritional protocol does not exist for IBS-D patients but it seems crucial to consider the effect of the different nutritional approaches on the intestinal microbiota composition to better define an efficient strategy to manage this functional disorder.     

Probiotics in functional bowel disorders

Functional bowel disorders (FBDs) are the most common gastrointestinal (GI) disorders seen by gastroenterologists and primary care physicians. The disorders affect patients functioning and quality of life (QOL) and are associated with significant healthcare burden. The current theory regarding the development of FBDs suggests brain-gut axis dysfunctions associated abnormal GI motility and sensation. Recent data suggest that alterations in the intestinal microbiota may have a role in the pathogenesis of FBDs; or at least have the potential to affect intestinal functions that are thought to be relevant to the development of functional GI symptoms. This has led to growing interest of healthcare providers and patients in targeting the intestinal microbiota for the treatment of FBDs. In this article we discuss the potential role probiotic interventions in the treatment of FBDs. We review the evidence from pre-clinical and clinical studies and discuss the current recommendations for the use of probiotics for FBDs in clinical practice.     

Molecular defects in mucosal serotonin content and decreased serotonin reuptake transporter in ulcerative colitis and irritable bowel syndrome

BACKGROUND & AIMS: Serotonin (5-HT) is a critical signaling molecule in the gut. 5-HT released from enterochromaffin cells initiates peristaltic, secretory, vasodilatory, vagal, and nociceptive reflexes. Despite being pathophysiologically divergent, ulcerative colitis (UC) and irritable bowel syndrome (IBS) are both associated with clinical symptoms that include alterations in the normal patterns of motility, secretion, and sensation. Our aim was to test whether enteric 5-HT signaling is defective in these disorders. METHODS: Rectal biopsy specimens were obtained from healthy controls and patients with UC, IBS with diarrhea (IBS-D), and IBS with constipation (IBS-C). Key elements of 5-HT signaling, including measures of 5-HT content, release, and reuptake, were analyzed with these samples. RESULTS: Mucosal 5-HT, tryptophan hydroxylase 1 messenger RNA, serotonin transporter messenger RNA, and serotonin transporter immunoreactivity were all significantly reduced in UC, IBS-C, and IBS-D. The enterochromaffin cell population was decreased in severe UC samples but was unchanged in IBS-C and IBS-D. When 5-HT release was investigated under basal and mechanical stimulation conditions, no changes were detected in any of the groups relative to controls. CONCLUSIONS: These data show that UC and IBS are associated with similar molecular changes in serotonergic signaling mechanisms. While UC and IBS have distinct pathophysiologic properties, these data suggest that shared defects in 5-HT signaling may underlie the altered motility, secretion, and sensation. These findings represent the first demonstration of significant molecular alterations specific to the gut in patients with IBS and support the assertion that disordered gastrointestinal function in IBS involves changes intrinsic to the bowel.     

Management Options for Irritable Bowel Syndrome

Irritable bowel syndrome (IBS) is associated with diverse pathophysiologic mechanisms. These mechanisms include increased abnormal colonic motility or transit, intestinal or colorectal sensation, increased colonic bile acid concentration, and superficial colonic mucosal inflammation, as well as epithelial barrier dysfunction, neurohormonal up-regulation, and activation of secretory processes in the epithelial layer. Novel approaches to treatment include lifestyle modification, changes in diet, probiotics, and pharmacotherapy directed to the motility, sensation, and intraluminal milieu of patients with IBS. Despite recent advances, there is a need for development of new treatments to relieve pain in IBS without deleterious central or other adverse effects.     

腹泻型肠易激综合征大鼠SCF/C-kit信号的变化及其与免疫功能的关系

目的探索腹泻型肠易激综合征(IBS-D)大鼠干细胞因子/酪氨酸激酶受体(SCF/C-kit)系统的变化及其与IBS-D免疫功能紊乱的相关性。方法 12只新生大鼠分为正常组和模型组,每组6只。模型组大鼠采用母婴分离、醋酸刺激、束缚应激三因素法制备IBS-D模型。免疫组化法检测两组大鼠结肠组织中SCF和C-kit的蛋白表达;q PCR法检测SCF和C-kit的mRNA表达;统计学分析SCF和C-kit的表达与IBS-D脾系数、胸腺系数、TNF-α、IL-8、IL-10的相关性。结果与正常组相比,模型组的SCF和C-kit的蛋白表达阳性率减少,同时二者的mRNA表达降低。SCF的表达与脾系数、TNF-α、IL-8呈负相关,与IL-10呈正相关;C-kit的表达与胸腺系数、脾系数、TNF-α呈负相关。结论 IBS-D大鼠SCF/C-kit系统异常,可能与IBS-D免疫功能紊乱有关。     

从“脾为之卫”浅析腹泻型肠易激综合征肠黏膜机械屏障损伤机制

肠黏膜机械屏障受损是腹泻型肠易激综合征(IBS-D)的重要病理生理基础,是目前的研究热点及新方向。“脾为之卫”是指脾具有抗御外邪、保护机体的作用,主要依托于“脾主运化”“脾主升清”而产生,“正气存内,邪不可干”是“脾为之卫”的主要内涵。从现代医学角度阐述,“脾为之卫”理论与肠黏膜机械屏障相通,是对于人体抵御外界有害物质侵袭功能的描述。脾气亏虚,正气不足,抗邪无力,湿邪内侵而致泄泻。脾气虚弱,肠黏膜机械屏障受损,有害物质通过肠黏膜直接作用于肠道而致腹痛、腹泻。现以“脾为之卫”为切入点,探讨脾虚型腹泻型肠易激综合征(IBS-D)肠黏膜机械屏障的损伤机制,为健脾益气法治疗IBS-D夯实理论基础,且为从“肠黏膜屏障”的角度治疗IBS-D提供理论依据。     

腹泻型肠易激综合征大鼠模型的建立

[目的]在传统束缚应激+番泻叶灌胃方法的基础上进行改良,旨在建立简便易行的腹泻型肠易激综合征大鼠模型.[方法]将大鼠随机分组,空白对照组(N)未做任何处理.单纯番泻叶组(F)灌服最佳浓度番泻叶水煎剂,不行束缚.单纯束缚组(S)灌服高压消毒饮用水,番泻叶联合束缚应激组(F+S)灌服最佳浓度番泻叶水煎剂,以上两组均行肢体束缚.观察各实验组体质量变化、排便情况等.[结果]N和S无稀便排出,而F、F+S两组均能排出不成形的稀软便,以F+S组明显(P<0.05).与N组相比较,其余3组大鼠平均体质量增长率均有显著性差异(P<0.01),尤以F+S呈明显负增长趋势(P<0.01).S与F+S可见免疫器官明显萎缩,脏体指数降低,与N、F两组相比较差异具有显著性(P<0.05).[结论]肢体束缚应激联合低浓度番泻叶灌胃方法,可以成功复制肠易激综合征(IBS-D)大鼠模型.