Impact of biologicals on faecal microbiota

The longitudinal impact of treatment with biologicals on the inflammatory burden and faecal microbiota in patients with Crohn’s disease (CD) and ulcerative colitis (UC) was studied. Biologicals resulted in a decrease in inflammation as reflected by faecal calprotectin (FCP) levels and an increase in microbial richness, but not in a shift in enterotypes [1].

At a tertiary referral centre, faecal samples were analysed of 349 patients with inflammatory bowel diseases (IBD; 112 UC, 237 CD) initiating a TNF inhibitor, vedolizumab, or ustekinumab between 2010 and 2019. Samples were collected at week 0, 14, and 24. The results showed a high diversity in faecal microbiota profiles, with samples classified into all 4 enterotypes: Bact1, Bact2, Prev, and Rum. Bact2 was 5- to 10-fold more prevalent in CD and UC patients compared with controls (see Figure). The variation in faecal microbiota composition was explained by diagnosis, timepoint, age, gender, and faecal moisture on multivariate analysis. The full model only explained 2.85% of the microbiota variation.

Figure: Enterotype prevalence in an average population cohort (Flemish Gut Flora Project: FGFP) and in UC and CD cohorts at week 0, 14, and 24 of treatment with TNF inhibitor, vedolizumab, or ustekinumab confounded [1]



Bact1, Bacteroides1; Bact2, Bacteroides2; Prev, Prevotella; Rum, Ruminococcus; UC, ulcerative colitis; CD, Crohn’s disease

Treatment was associated with a significant decrease in FCP concentrations, along with a significant increase in cell counts. Bact2 prevalence did not significantly change during treatment. Treatment response was not significantly predicted by microbiota-associated variables (enterotype, cell counts, and faecal moisture), but only by treatment-associated variables (week of treatment, P<0.0001; diagnosis, P=0.0005; and timepoint, P=0.0073). Baseline samples were associated with higher FCP levels. This suggests that the response time of the microbiota to treatment is longer than the host inflammatory response.

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   1. Caenepeel C, et al. ECCO-IBD 2020, OP20.

Posted on 14 April 202023 April 2024