Carstens A 1,2, Dicksved J 3, Nelson R 4, Andréasson A 5, 6, 7, Bohr J, 2, Tysk C 2, Agréus L 6, Engstrand L 5, Halfvarson J 2
1Department of Internal Medicine, Ersta Hospital, Stockholm, Sweden. 2Department of Gastroenterology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden. 3Department of Animal Nutrition and Management, Swedish University of Agricultural Sciences, Uppsala, Sweden. 4Department of Clinical Sciences, Swedish University of Agricultural Sciences, Uppsala, Sweden. 5Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institute, Solna, Sweden. 6Centre for Family Medicine, Karolinska Institute, Solna, Sweden. 7Stress Research Institute, Stockholm University, Stockholm, Sweden.
Similar to inflammatory bowel diseases (IBD), an aberrant immune response to luminal factors, such as the gut microbiota, seems to play a key role in the pathophysiology of collagenous colitis (CC). We aimed to characterize the fecal microbiota of CC in comparison to healthy controls (HC) and to explore shared features with Crohn’s disease (CD) and ulcerative colitis (UC). Moreover, we wanted to assess the influence of disease activity and corticosteroid treatment on the fecal microbiome of CC.
Fecal samples were collected from patients at the out-patient clinic; CC (n=29) and HC, (n=29) as well as UC (n=32), CD (n=32). DNA was extracted and amplicons of the hypervariable V3-V4 regions of the 16S rRNA gene were analyzed using next-generation sequencing. Shannon diversity index and ANOSIM were used to compare phenotypes. Differences in abundance of taxa between groups of patients were analyzed by Wilcoxon’s test. Kruskal Wallis and Mann-Whitney U were used to further categorize shifts in active or inactive disease. False discovery rate was applied to adjust for multiple comparisons.
There was no difference in Shannon diversity index between patients with CC and HC (p=0.54). ANOSIM showed that the CC group segregated from the HC with higher taxonomic resolution (p=0.03 at operational taxonomic unit level). Several taxa belonging to the Ruminococcaceae family were underrepresented in the CC group compared to HC. CC patients with active disease showed a lower relative abundance of 10 taxa belonging to the Ruminococcaceae family of which 9 was lower in CD and 4 in UC.
Fecal microbiota of CC differs from HC and is characterized by a lower abundance of taxa belonging to the Ruminococcaceae family. Underrepresentation of the Ruminococcaceae family has previously been associated with IBD, indicating that the fecal microbiota in CC shares characteristics with changes seen in IBD.