Abstract
The biogeography of inflammation in ulcerative colitis (UC) suggests a proximal to distal concentration gradient of a toxin. Hydrogen sulfide (H2S) has long been considered one such toxin candidate, and dietary sulfur along with the abundance of sulfate reducing bacteria (SRB) were considered the primary determinants of H2S production and clinical course of UC. The metabolic milieu in the lumen of the colon, however, is the result of a multitude of factors beyond dietary sulfur intake and SRB abundance. Here we present an updated formulation of the H2S toxin hypothesis for UC pathogenesis, which strives to incorporate the interdependency of diet composition and the metabolic activity of the entire colon microbial community. Specifically, we suggest that the increasing severity of inflammation along the proximal-to-distal axis in UC is due to the dilution of beneficial factors, concentration of toxic factors, and changing detoxification capacity of the host, all of which are intimately linked to the nutrient flow from the diet.
Highlights
Inflammatory bowel disease (IBD), which includes both Crohn’s disease and ulcerative colitis (UC), is estimated to affect ~3 million individuals in the U.S alone and continues to increase in incidence and prevalence worldwide [1]
The underlying mechanisms that make up the H2 S toxin hypothesis are supported by changes produced with fermentable fiber supplementation in individuals with UC [144] and findings from a recent fecal microbial transplantation (FMT) trial that demonstrated a correlation between sustained remission and increased butyrate production, while increased abundances of Bacteroidetes and Proteobacteria correlated with no response or relapse [122]
There is an intriguing body of literature supporting a relationship between dietary sulfur intake and the H2 S toxin hypothesis in the development of UC
Summary
Inflammatory bowel disease (IBD), which includes both Crohn’s disease and ulcerative colitis (UC), is estimated to affect ~3 million individuals in the U.S alone and continues to increase in incidence and prevalence worldwide [1]. UC, an emphasis approach has been theoffocus of adietary number of recent (e.g., reviews [16,17], preliminary suggest should be placed on overall diet patterns (e.g.,may animalvs plant-based diet) This approach has been that these types of compositional dietary changes be beneficial in IBD [18]. The updated understanding of the H2 S toxin hypothesis for UC pathogenesis presented here strives to account for the activity of the entire microbial community rather than individual microbial subgroups working in isolation (e.g., Desulfovibrio) and appreciates the interdependency of diet composition on both the structure and function of the microbial community In many respects, this is a synecological approach to study of the relationship between gut microbiota and the development of UC
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
