Background: 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.
Methods: 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.
Results: 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.
Conclusions: 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.
Article first published online 30 July 2013
*Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical University of Graz, Graz, Austria;
†Department of Internal Medicine, Barmherzige Brüder Hospital, St. Veit an der Glan, Austria;
‡Center for Medical Research, Medical University of Graz, Graz, Austria;
§Department of Internal Medicine, Barmherzige Brüder Hospital, Graz, Austria;
‖Department of Pediatrics, Medical University of Graz, Graz, Austria; and
¶Institute of Pathology, Medical University of Graz, Graz, Austria.
Reprints: Christoph Högenauer, MD, Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria (e-mail: email@example.com); Gregor Gorkiewicz, MD, Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25, 8036 Graz, Austria (e-mail: firstname.lastname@example.org).
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Supported by the regular scientific budget of the Division of Gastroenterology and Hepatology, Medical University of Graz.
The authors have no conflicts of interest to disclose.
Received May 17, 2013
Accepted June 2, 2013