Alteration of Intestinal Dysbiosis by Fecal Microbiota Transplantation Does not Induce Remission in Patients with Chronic Active Ulcerative Colitis

溃疡性结肠炎 粪便细菌疗法 失调 医学 胃肠病学 粪便 炎症性肠病 移植 结肠炎 内科学 免疫学 肠道菌群 艰难梭菌 生物 微生物学 抗生素 疾病
作者
Patrizia Kump,H Gröchenig,Stefan Lackner,Slave Trajanoski,G Reicht,K. Martin Hoffmann,Andrea Deutschmann,H Wenzl,Wolfgang Petritsch,Guenter J. Krejs,Gregor Gorkiewicz,Christoph Högenauer
出处
期刊:Inflammatory Bowel Diseases [Oxford University Press]
卷期号:19 (10): 2155-2165 被引量:232
标识
DOI:10.1097/mib.0b013e31829ea325
摘要

In patients with ulcerative colitis (UC), alterations of the intestinal microbiota, termed dysbiosis, have been postulated to contribute to intestinal inflammation. Fecal microbiota transplantation (FMT) has been used as effective therapy for recurrent Clostridium difficile colitis also caused by dysbiosis. The aims of the present study were to investigate if patients with UC benefit from FMT and if dysbiosis can be reversed.Six patients with chronic active UC nonresponsive to standard medical therapy were treated with FMT by colonoscopic administration. Changes in the colonic microbiota were assessed by 16S rDNA-based microbial community profiling using high-throughput pyrosequencing from mucosal and stool samples.All patients experienced short-term clinical improvement within the first 2 weeks after FMT. However, none of the patients achieved clinical remission. Microbiota profiling showed differences in the modification of the intestinal microbiota between individual patients after FMT. In 3 patients, the colonic microbiota changed toward the donor microbiota; however, this did not correlate with clinical response. On phylum level, there was a significant reduction of Proteobacteria and an increase in Bacteroidetes after FMT.FMT by a single colonoscopic donor stool application is not effective in inducing remission in chronic active therapy-refractory UC. Changes in the composition of the intestinal microbiota were significant and resulted in a partial improvement of UC-associated dysbiosis. The results suggest that dysbiosis in UC is at least in part a secondary phenomenon induced by inflammation and diarrhea rather than being causative for inflammation in this disease.
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