Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases

溃疡性结肠炎 炎症性肠病 厚壁菌 发病机制 拟杆菌 生物 节点2 胃肠道 疾病 微生物学 免疫学 克罗恩病 细菌 医学 病理 16S核糖体RNA 遗传学 生物化学
作者
Daniel N. Frank,Allison L. St. Amand,Robert A. Feldman,Edgar C. Boedeker,Noam Harpaz,Norman R. Pace
出处
期刊:Proceedings of the National Academy of Sciences of the United States of America [Proceedings of the National Academy of Sciences]
卷期号:104 (34): 13780-13785 被引量:3825
标识
DOI:10.1073/pnas.0706625104
摘要

The two primary human inflammatory bowel diseases, Crohn's disease (CD) and ulcerative colitis (UC), are idiopathic relapsing disorders characterized by chronic inflammation of the intestinal tract. Although several lines of reasoning suggest that gastrointestinal (GI) microbes influence inflammatory bowel disease (IBD) pathogenesis, the types of microbes involved have not been adequately described. Here we report the results of a culture-independent rRNA sequence analysis of GI tissue samples obtained from CD and UC patients, as well as non-IBD controls. Specimens were obtained through surgery from a variety of intestinal sites and included both pathologically normal and abnormal states. Our results provide comprehensive molecular-based analysis of the microbiota of the human small intestine. Comparison of clone libraries reveals statistically significant differences between the microbiotas of CD and UC patients and those of non-IBD controls. Significantly, our results indicate that a subset of CD and UC samples contained abnormal GI microbiotas, characterized by depletion of commensal bacteria, notably members of the phyla Firmicutes and Bacteroidetes . Patient stratification by GI microbiota provides further evidence that CD represents a spectrum of disease states and suggests that treatment of some forms of IBD may be facilitated by redress of the detected microbiological imbalances.
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