Pfeffer-Gik Tamar, Levine Arie
PIBD Research Center, Tel Aviv University, Tel Aviv, and Pediatric Gastroenterology and Nutrition Unit, E. Wolfson Medical Center, Holon, Israel.
Dig Dis. 2014;32(4):389-94. doi: 10.1159/000358143. Epub 2014 Jun 23.
Crohn's disease is a complex inherited disorder of unknown pathogenesis with environmental, genetic and microbial factors involved in the development of the disease. A remarkable feature of this disease in childhood is the effective response to exclusive enteral nutrition (EEN) therapy and the need for complete exclusion of normal diet required for success (principle of exclusivity). EEN or dietary interventions might act through removal of dietary components, which affect microbial composition, decrease a proinflammatory response and promote restitution of the epithelial barrier, likewise allowing termination of this vicious disease-forming cycle before a critical threshold is reached. Multiple traditional and nontraditional dietary components may affect the microbiome, mucous layer, intestinal permeability, or adherence and translocation of pathobionts. We review the epidemiological data, as well as data from animal models and cell lines, and propose a model for pathogenesis we have termed the 'bacterial penetration cycle', whereby dietary components such as animal fat, high sugar intake and gliadin, and consumption of emulsifiers, maltodextrin as well as low-fiber diets may be able to cause a localized acquired bacterial clearance defect, leading to bacterial adhesion and penetration, and subsequently inflammation in the gut.
克罗恩病是一种发病机制不明的复杂遗传性疾病，环境、遗传和微生物因素均参与该疾病的发生发展。儿童期这种疾病的一个显著特征是对全肠内营养（EEN）疗法有有效反应，且成功治疗需要完全排除正常饮食（排他性原则）。EEN或饮食干预可能通过去除影响微生物组成、降低促炎反应并促进上皮屏障修复的饮食成分来发挥作用，同样也能在达到临界阈值之前终止这种形成疾病的恶性循环。多种传统和非传统饮食成分可能会影响微生物群、黏液层、肠道通透性，或致病菌的黏附和易位。我们回顾了流行病学数据以及来自动物模型和细胞系的数据，并提出了一种发病机制模型，我们将其称为“细菌穿透循环”，即动物脂肪、高糖摄入、麦醇溶蛋白等饮食成分，以及食用乳化剂、麦芽糊精和低纤维饮食可能会导致局部获得性细菌清除缺陷，从而导致细菌黏附和穿透，进而引发肠道炎症。
