Fecal microbiota transplants (FMT) work when it comes to treating Clostridium difficile colitis as it restores alterations in the intestinal microbiota. But is dysbiosis responsible for intestinal inflammation in inflammatory bowel dieases such as ulcerative colitis (UC)? This question has created a lot of buzz and is the focus of next week’s human microbiome jounal club! As I learned this week (courtesy of my lab mate Julie Kaiser @jukais), many people with UC do think FMT is the answer and has taken it upon them to create and administer a home made stool cocktail – a movement now dubbed DIY fecal transplants http://bit.ly/12iRb93 .
Join us Thursday August 29 at 3 pm at the Phoenix to discuss Kump et al., 2013 – a study that concludes intestinal dysbiosis in UC patients does not cause inflammation but is a result of inflammation.
Some points we could discuss:
- Is dysbiosis in UC a cause of inflammation or a result?
- Are 6 patients enough to make a statistically significant conclusion?
- How big a role do donors play in UC FMT success? Could sex, age and environment play a role in a donor’s success?
- The authors used a single application of donor stool – why does it work for C. Diff but not UC
- DIY FMT – good idea?
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.