A decrease of the butyrate-producing species Roseburia hominis and Faecalibacterium prausnitzii defines dysbiosis in patients with ulcerative colitis.

Machiels et al. recently described that the composition of the faecal microbiota of patients suffering from ulcerative colitis differs from that of healthy individuals: they found a reduction in two well-known butyrate-producing bacteria of the Firmicutes phylum, Roseburia hominis and Faecalibacterium prausnitzii. This has been confirmed in other studies. The dysbiosis found in the two inflammatory bowel diseases (IBD) i.e. Crohn’s disease and ulcerative colitis share common characteristics but also specificities. Such discoveries will soon help establishing new diagnostic tools and preliminary data are encouraging.  These tools will receive a high interest from clinicians as they will improve the diagnosis in difficult cases, especially at early stages of the disease when treatments are usually more effective. Studies in families and follow up studies are also expected to provide major breakthroughs. As these bacteria are butyrate producers, the “old idea” of trying to improve butyrate production during IBD by various means is still very rational. One should also try to decipher the role of diet, especially low in fiber, in the dysbiosis. Obviously this is an important topic to follow for gastroenterologists and ecologists.

Machiels K, Joossens M, Sabino J, De Preter V, Arijs I, Eeckhaut V, Ballet V, Claes K, Van Immerseel F, Verbeke K, Ferrante M, Verhaegen J, Rutgeerts P, Vermeire S. A decrease of the butyrate-producing species Roseburia hominis and Faecalibacterium prausnitzii defines dysbiosis in patients with ulcerative colitis. Gut. 2013 Sep 10. doi: 10.1136/gutjnl-2013-304833.

[Abstract]

Objective Bacteria play an important role in the onset and perpetuation of intestinal inflammation in inflammatory bowel disease (IBD). Unlike in Crohn’s disease (CD), in which dysbiosis has been better characterised, in ulcerative colitis (UC), only small cohorts have been studied and showed conflicting data. Therefore, we evaluated in a large cohort if the microbial signature described in CD is also present in UC, and if we could characterise predominant dysbiosis in UC. To assess the functional impact of dysbiosis, we quantified the bacterial metabolites.

Design The predominant microbiota from 127 UC patients and 87 age and sex-matched controls was analysed using denaturing gradient gel electrophoresis (DGGE) analysis. Differences were quantitatively validated using real-time PCR. Metabolites were quantified using gas chromatography–mass spectrometry.

Results Based on DGGE analysis, the microbial signature previously described in CD was not present in UC. Real-time PCR analysis revealed a lower abundance of Roseburia hominis (p<0.0001) and Faecalibacterium prausnitzii (p<0.0001) in UC patients compared to controls. Both species showed an inverse correlation with disease activity. Short-chain fatty acids (SCFA) were reduced in UC patients (p=0.014), but no direct correlation between SCFA and the identified bacteria was found.

Conclusions The composition of the fecal microbiota of UC patients differs from that of healthy individuals: we found a reduction in R hominis and F prausnitzii, both well-known butyrate-producing bacteria of the Firmicutes phylum. These results underscore the importance of dysbiosis in IBD but suggest that different bacterial species contribute to the pathogenesis of UC and CD.