Exploring the microbiological basis of ulcerative colitis as an energy deficiency disease
Earley H1,2., Lennon G1,2., Balfe A1,2., Lavelle A1,2., Coffey JC 3., Winter DC2., O’Connell PR1,2
1. School of Medicine and Medical Science, University College Dublin. 2. Centre for Colorectal Disease, St. Vincent’s University Hospital, Dublin. 3. GEMS, University of Limerick.
The short chain fatty acid (SCFA) butyrate is the primary energy source for the colonic mucosa. Reduced abundance of this SCFA has been reported in the setting of ulcerative colitis (UC) and a lack of butyrate has been proposed as a potential aetiological factor in colonic inflammation. Commensal microbes, such as F. prausnitzii are involved in the production of butyrate. Other commensals are thought to have an inhibitory effect on butyrate, possibly through the production of toxic metabolites. One such metabolite is Hydrogen sulphide (H2S), believed to inhibit buyrate oxidation.
This study aimed to determine the relative abundance of butyrogenic F. pruasnitzii and microbes with the ability to produce H2S (Desulfobacter, Desulfobulbus and Bilophila wadsworthia) within the MGL of the colitic colon.
Paired mucosal brushings and biopsies were obtained from a cohort of 20 patients with active colitis and healthy controls and 14 patients with quiescent colitis. RT-PCR specific for F. prausnitzii, Desulfobacter, Desulfobulbus and B. wadsworthia was used to determine the abundance of each bacterial target in the MGL.
F. pruasnitzii was significantly more abundant in health compared to quiescent and active UC. The H2S-producing B. wadsworthia species was reduced in UC. No difference in the abundance of Desulfobulbus and Desulfobacter was observed between cohorts.
These data suggest that the reported deficiency of colonic butyrate in the setting of UC may be due to a primary deficiency, related to reduced microbial butyrate production, rather than inhibition of butyrate oxidation by microbial by-products.