Why are disorders of gut-brain interaction (DGBI) often food-related? Duodenal eosinophils and mast cells, small intestinal bacteria, food allergy and altered food intake in functional dyspepsia and the irritable bowel syndrome: a new paradigm.

IF 6.9 2区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Nicholas J Talley, Kerith Duncanson, Georgina M Williams
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引用次数: 0

Abstract

The underlying causes of irritable bowel syndrome (IBS) and functional dyspepsia (FD) have remained largely elusive, but emerging data suggest immune activation and loss of small intestinal homeostasis may explain a major subgroup. FD and IBS symptoms often overlap and may occur early in the post-prandial period, suggesting the origin of symptoms may be much higher in gastrointestinal tract than colon. There is strong evidence low-grade duodenal inflammation, comprising eosinophils and/or mast cells associated with increased permeability, is present at least in a major subset with FD and IBS. This hypothesis is further supported by evidence of circulating increased small intestinal homing T cells and altered duodenal microbiota. We hypothesize a major etiologic pathway whereby interaction of food with intestinal bacteria switches on small intestinal immune activation in FD and IBS leading to presentation of antigens to the mucosa. While the low FODMAP diet provides symptom relief in both IBS and FD, this diet notably also reduces common food protein antigens (e.g., wheat, milk, soy) and urinary histamine levels. The obvious but often overlooked fact that food ingestion usually requires the act of eating adds nuance to determining whether food components or eating itself induces symptoms and that both need to be considered in DGBI in clinical practice. The exciting observations about subtle inflammation in DGBIs offer hope for new diagnostic biomarkers, and if considered in the context of altered dietary patterns and validated against symptom responses, will pave the way for novel DGBI treatment options.

为什么肠脑相互作用紊乱(DGBI)经常与食物有关?十二指肠嗜酸性粒细胞和肥大细胞,小肠细菌,食物过敏和食物摄入改变在功能性消化不良和肠易激综合征:一个新的范式。
肠易激综合征(IBS)和功能性消化不良(FD)的根本原因在很大程度上仍然难以理解,但新出现的数据表明,免疫激活和小肠稳态的丧失可能解释了一个主要的亚群。FD和IBS症状经常重叠,并可能出现在餐后早期,提示症状的胃肠道起源可能远高于结肠。有强有力的证据表明,至少在FD和IBS的主要亚群中存在低度十二指肠炎症,包括嗜酸性粒细胞和/或肥大细胞,并伴有通透性增加。这一假设进一步得到了循环增加的小肠归巢T细胞和改变的十二指肠微生物群的证据的支持。我们假设了一个主要的病因途径,即食物与肠道细菌的相互作用在FD和IBS中开启小肠免疫激活,导致抗原呈递到粘膜。虽然低FODMAP饮食可以缓解肠易激综合征和FD的症状,但这种饮食也显著降低了常见的食物蛋白抗原(如小麦、牛奶、大豆)和尿组胺水平。食物摄入通常需要进食这一明显但经常被忽视的事实,增加了确定食物成分或进食本身是否会引起症状的细微差别,并且在DGBI临床实践中需要考虑这两者。关于DGBI中细微炎症的令人兴奋的观察结果为新的诊断生物标志物提供了希望,如果在改变饮食模式的背景下考虑并根据症状反应进行验证,将为新的DGBI治疗选择铺平道路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Gastroenterology
Journal of Gastroenterology 医学-胃肠肝病学
CiteScore
12.20
自引率
1.60%
发文量
99
审稿时长
4-8 weeks
期刊介绍: The Journal of Gastroenterology, which is the official publication of the Japanese Society of Gastroenterology, publishes Original Articles (Alimentary Tract/Liver, Pancreas, and Biliary Tract), Review Articles, Letters to the Editors and other articles on all aspects of the field of gastroenterology. Significant contributions relating to basic research, theory, and practice are welcomed. These publications are designed to disseminate knowledge in this field to a worldwide audience, and accordingly, its editorial board has an international membership.
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