Lee Goo, Buchman Alan L
Division of Gastroenterology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Nutrition. 2009 Sep;25(9):885-91. doi: 10.1016/j.nut.2009.06.011.
Inflammatory bowel disease (IBD) consists of two main disorders, ulcerative colitis and Crohn's disease, that cause chronic, recurrent inflammation of the intestine. An inappropriate immune response to the enteric ecosystem has been postulated to cause IBD. Genomewide association studies provide the information of diverse genetic variations and susceptibilities to patients with IBD. Through the application of these studies, the pathogenesis of IBD may result in part from genetic abnormalities that regulate epithelial barrier function and innate and adaptive immune responses. Crohn's disease shows strong association with CARD15, ATG15L1, and IRGM, which are involved in the innate immunity. In the adaptive immune response, IL23R, MST1, IL12B, and STAT3 polymorphisms are associated with Crohn's disease and ulcerative colitis. Current pharmacologic treatment of IBD, including 5-aminosalycylate, steroids, and immunomodulator therapy, are mainly aimed at suppressing inflammation non-specifically, except biologic therapies such as anti-tumor necrosis factor molecule, which block specific proinflammatory molecules. For nutritional issues in IBD, the mainstay of therapy has been supportive, with particular attention paid to the prevention, recognition, and therapy of nutritional deficiencies, and individual outcomes to specific dietary factors have been controversial. Parenteral nutritional support and exclusionary diets have been investigated and are not the subject of this review. The emerging concepts of nutrition-gene interaction gave birth to unique scientific fields, nutrigenetics and nutrigenomics. These studies provide information about 1) the genetic variability that induces an individual's response to nutrition according to particular states of health and disease and 2) changes in gene expression that develop as a result of nutrition-gene interaction. For IBD, the role of diet in the regulation of the immune response against gut flora is the subject of current intensive evaluation. These approaches may lead clinicians to derive a personalized nutritional prescription based on individual genetic variations and may result in a significant impact on IBD treatment.
炎症性肠病（IBD）主要包括两种疾病，即溃疡性结肠炎和克罗恩病，它们会导致肠道的慢性复发性炎症。据推测，对肠道生态系统的不适当免疫反应会引发IBD。全基因组关联研究为IBD患者提供了多种基因变异和易感性信息。通过应用这些研究，IBD的发病机制可能部分源于调节上皮屏障功能以及先天性和适应性免疫反应的基因异常。克罗恩病与参与先天性免疫的CARD15、ATG15L1和IRGM密切相关。在适应性免疫反应中，IL23R、MST1、IL12B和STAT3基因多态性与克罗恩病和溃疡性结肠炎相关。IBD目前的药物治疗，包括5-氨基水杨酸、类固醇和免疫调节剂治疗，主要旨在非特异性地抑制炎症，但生物疗法如抗肿瘤坏死因子分子除外，其可阻断特定的促炎分子。对于IBD中的营养问题，治疗的主要方式一直是支持性的，特别关注营养缺乏的预防、识别和治疗，而特定饮食因素的个体结果一直存在争议。肠内营养支持和排除性饮食已被研究，但并非本综述的主题。营养-基因相互作用的新兴概念催生了独特的科学领域，即营养遗传学和营养基因组学。这些研究提供了以下信息：1）根据健康和疾病的特定状态诱导个体对营养反应的基因变异性；2）营养-基因相互作用导致的基因表达变化。对于IBD，饮食在调节针对肠道菌群的免疫反应中的作用是当前深入评估的主题。这些方法可能会引导临床医生根据个体基因变异制定个性化的营养处方，并可能对IBD治疗产生重大影响。
