Publisher Information: Örebro universitet, Institutionen för medicinska vetenskaper Örebro universitet, Institutionen för hälsovetenskaper Region Örebro län Department of Internal Medicine, Ersta Hospital, Stockholm, Sweden; Department of Gastroenterology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden Department of Animal Nutrition and Management, Swedish University of Agricultural Sciences, Uppsala, Sweden Department of Clinical Sciences, Swedish University of Agricultural Sciences, Uppsala, Sweden Division of Family Medicine and Primary Care, Karolinska Institutet, Huddinge, Sweden Department of Gastroenterology Department of Gastroenterology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden Faculty of Medicine and Health, University of Newcastle, Newcastle, Australia Division of Family Medicine and Primary Care, Karolinska Institutet, Huddinge, Sweden Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Solna, Sweden Department of Gastroenterology 2019
نبذة مختصرة : INTRODUCTION: In inflammatory bowel disease (IBD), an aberrant immune response to gut microbiota is important, but the role of the microbiota in collagenous colitis (CC) is largely unknown. We aimed to characterize the microbiota of patients with CC compared with that of healthy control and patients with IBD. METHODS: Fecal samples were collected from patients with CC (n = 29), age- and sex-matched healthy controls (n = 29), patients with Crohn's disease (n = 32), and patients with ulcerative colitis (n = 32). Sequence data were obtained by 454 sequencing of 16S rRNA gene amplicons, and the obtained sequences were subsequently taxonomically classified. RESULTS: Analysis of similarity statistics showed a segregation between patients with CC and healthy controls with increasing taxonomic resolution, becoming significant comparing operational taxonomic unit data (P = 0.006). CC had a lower abundance of 10 different taxa. Taxa-specific analyses revealed a consistent lower abundance of several operational taxonomic units belonging to the Ruminococcaceae family in patients with CC, q < 0.05 after false discovery rate correction. Loss of these taxa was seen in patients with CC with active disease and/or corticosteroid treatment only and resembled the findings in patients with IBD. DISCUSSION: CC is associated with a specific fecal microbiome seen primarily in patients with active disease or ongoing corticosteroid treatment, whereas the microbiome of CC patients in remission resembled that of healthy controls. Notably, the shift in key taxa, including the Ruminococcaceae family, was also observed in IBD. There may be common mechanisms in the pathogenesis of CC and IBD.
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