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P373. Faecalibacterium prausnitzii is also reduced in ulcerative colitis

P373. Faecalibacterium prausnitzii is also reduced in ulcerative colitis

K. Machiels, M. Joossens, V. De Preter, I. Arijs, V. Ballet, S. Organe, T. Coopmans, G. Van Assche, J. Verhaegen, P. Rutgeerts, S. Vermeire

UZ Gasthuisberg, Leuven, Belgium

Aims: In Crohn's disease, intestinal dysbiosis has been demonstrated with an important reduction of Faecalibacterium prausnitzii, a commensal with anti-inflammatory properties, as most replicated species-specific finding so far. In ulcerative colitis (UC) patients, a decrease in intestinal biodiversity might be present. However, only limited data on the importance of F. prausnitzii in UC is available.

We hypothesized that F. prausnitzii is reduced in fecal samples of UC patients as compared to healthy subjects and studied the influence of disease activity on the amount of F. prausnitzii.

Materials and Methods: Fecal samples were collected from 83 UC patients (26 active UC (A-UC), 57 remission UC (R-UC)) and 43 healthy subjects (HS). Disease activity in UC was defined using the partial Mayo score. Written consent was given by all participants prior to collection of the samples. Participants were excluded if they had used antibiotics or probiotics in the last month. Bacterial DNA was extracted by a modification of the method of Pitcher et al (Letters in Applied Microbiology 1989). Quantification of F. prausnitzii was performed by real-time PCR targeting the 16S rRNA gene in the V3 region. Bacterial counts were expressed as log10 values per gram wet weight feces. Results were analyzed with the Mann-Whitney U-test and the Spearman's correlation coefficient using SPSS 17.0 software. A p-value of <0.05 was considered significant.

Results: The bacterial count of F. prausnitzii in UC patients was significantly lower (median 10.7, interquartile range (IQR) 9.6–11.7) as compared to HS (median 11.5; IQR 11.2–12.0) (p < 0.001). We further more observed a correlation between the amount of F. prausnitzii and disease activity. F. prausnitzii was decreased according disease activity. Bacterial count was lowest in UC patients with severe disease (median 9.7; IQR 8.1–10.8; Mayo 3; number 10) as compared to moderate disease (median, 10.6; IQR 8.7–11.5; Mayo 2; number 16) and quiescent disease (median 11.0; IQR 9.8–11.7; Mayo 0+1; number 57) (Spearman's r = −0.241, p = 0.028) (Figure 1).

Conclusion: A significant underrepresentation of F. prausnitzii was observed in UC patients when compared to healthy controls. Disease activity even further decreased the bacterial count. Our results suggest that dysbiosis plays also a role in UC pathogenesis, and in particular points to the protective effects of F. prausnitzii against inflammation.

Figure 1. Comparison between healthy subjects (HS) and UC patients according to disease activity.