Sartor R Balfour, Wu Gary D
Departments of Medicine, Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Division of Gastroenterology, Perelman School of Medicine, the University of Pennsylvania, Philadelphia, Pennsylvania.
Gastroenterology. 2017 Feb;152(2):327-339.e4. doi: 10.1053/j.gastro.2016.10.012. Epub 2016 Oct 18.
Intestinal microbiota are involved in the pathogenesis of Crohn's disease, ulcerative colitis, and pouchitis. We review the mechanisms by which these gut bacteria, fungi, and viruses mediate mucosal homeostasis via their composite genes (metagenome) and metabolic products (metabolome). We explain how alterations to their profiles and functions under conditions of dysbiosis contribute to inflammation and effector immune responses that mediate inflammatory bowel diseases (IBD) in humans and enterocolitis in mice. It could be possible to engineer the intestinal environment by modifying the microbiota community structure or function to treat patients with IBD-either with individual agents, via dietary management, or as adjuncts to immunosuppressive drugs. We summarize the latest information on therapeutic use of fecal microbial transplantation and propose improved strategies to selectively normalize the dysbiotic microbiome in personalized approaches to treatment.
肠道微生物群参与克罗恩病、溃疡性结肠炎和袋炎的发病机制。我们综述了这些肠道细菌、真菌和病毒通过其复合基因（宏基因组）和代谢产物（代谢组）介导黏膜稳态的机制。我们解释了在生态失调情况下它们的谱和功能改变如何导致炎症以及介导人类炎症性肠病（IBD）和小鼠小肠结肠炎的效应免疫反应。通过改变微生物群群落结构或功能来改造肠道环境以治疗IBD患者是有可能的——可以使用单一药物、通过饮食管理或作为免疫抑制药物的辅助手段。我们总结了粪便微生物移植治疗用途的最新信息，并提出改进策略，以便在个性化治疗方法中选择性地使失调的微生物组正常化。
