The role of duodenal microbiota in ulcerative colitis

Actu PRO Le microbiote duodénal impliqué dans la rectocolite hémorragique

In children with ulcerative colitis, the duodenal microbiota shows significant anomalies that suggest it is involved in colon inflammation.


Intestinal dysbioses are associated with chronic inflammatory bowel disease (CIBD). Until now, data was only available regarding the microbiota of the colon and terminal ileum. However, that of the proximal part of the small intestine may also be involved in colonic inflammation, which is a major issue in cases of ulcerative colitis. The microbiota of the small intestine plays a role in the regulation of local and systemic immunity and in the tolerance to microorganisms and antigens present in the gastrointestinal tract.

Researchers analyzed children’s duodenal microbiota in duodenal fluid samples extracted before carrying out biopsies as part of CIBD screening tests. They then compared the composition between subjects who had ulcerative colitis (n=8), Crohn’s disease (n=5) and those without CIBD (n=8). Children with ulcerative colitis had a duodenal microbiota that differed from that of healthy subjects. It showed reduced bacterial diversity, with a significant depletion of Firmicutes, Actinobacteria, and Bacteroidetes. Several bacterial genera were also present in scarse amounts: Collinsella, Lactobacillus, Bacillus, and an unidentified genus belonging to the order Sphingobacteriales. According to the study’s authors, lower bacterial diversity could be explained by limited exposure to microorganisms through diet or the environment. This hypothesis is in line with the observation that there is an increased prevalence of CIBD in countries with high levels of hygiene. In children with Crohn’s disease, bacterial diversity also seemed to be reduced, but the results varied within the group and the differences were not significant.



Sjöberg F et al. Low-complexity microbiota in the duodenum of children with newly diagnosed ulcerative colitis. PLoS One. 2017 Oct 19;12(10):e0186178.