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Clin Exp Gastroenterol. 2019 Jan 31;12:37-49. doi: 10.2147/CEG.S186235. eCollection 2019.

Fecal microbiota profiles in treatment-naïve pediatric inflammatory bowel disease - associations with disease phenotype, treatment, and outcome.

Author information

Department of Pediatric and Adolescent Medicine, Akershus University Hospital, Lørenskog, Norway,
Institute of Clinical Medicine, Campus Ahus, University of Oslo, Oslo, Norway,
Faculty of Health Sciences, Oslo Metropolitan University, Oslo, Norway.
Department of Gastroenterology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Department of Clinical Molecular Biology (EpiGen), Division of Medicine, Akershus University Hospital, Lørenskog, and University of Oslo, Oslo, Norway.
Department of Gastroenterology, Akerhus University Hospital, Lørenskog, Norway.
Institute of Clinical Medicine, University of Oslo, Health Services Research Unit, Akershus University Hospital, Lørenskog, Norway.
Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
Department of Clinical and Experimental Medicine, Faculty of Medicine and Health Sciences, Linköping University, Linköping, Sweden.
Digestive Diseases Unit, IIS Aragón, Zaragoza, Spain.
Genetic-Analysis AS, Oslo, Norway.
Gastrointestinal Unit, Centre for Genomics and Molecular Medicine, University of Edinburgh, Edinburgh, UK.
Translational Gastroenterology Unit, Experimental Medicine Division, University of Oxford, Oxford, UK.
Department of Pediatrics, Oslo University Hospital, Ullevål, Oslo, Norway.



Imbalance in the microbiota, dysbiosis, has been identified in inflammatory bowel disease (IBD). We explored the fecal microbiota in pediatric patients with treatment-naïve IBD, non-IBD patients with gastrointestinal symptoms and healthy children, its relation to IBD subgroups, and treatment outcomes.

Patients and methods:

Fecal samples were collected from 235 children below 18 years of age. Eighty children had Crohn's disease (CD), 27 ulcerative colitis (UC), 3 IBD unclassified, 50 were non-IBD symptomatic patients, and 75 were healthy. The bacterial abundance of 54 predefined DNA markers was measured with a 16S rRNA DNA-based test using GA-Map technology at diagnosis and after therapy in IBD patients.


Bacterial abundance was similarly reduced in IBD and non-IBD patients in 51 of 54 markers compared to healthy patients (P<0.001). Only Prevotella was more abundant in patients (P<0.01). IBD patients with ileocolitis or total colitis had more Ruminococcus gnavus (P=0.02) than patients with colonic CD or left-sided UC. CD patients with upper gastrointestinal manifestations had higher Veillonella abundance (P<0.01). IBD patients (58%) who received biologic therapy had lower baseline Firmicutes and Mycoplasma hominis abundance (P<0.01) than conventionally treated. High Proteobacteria abundance was associated with stricturing/penetrating CD, surgery (P<0.01), and nonmucosal healing (P<0.03). Low Faecalibacterium prausnitzii abundance was associated with prior antibiotic therapy (P=0.001), surgery (P=0.02), and nonmucosal healing (P<0.03). After therapy, IBD patients had unchanged dysbiosis.


Fecal microbiota profiles differentiated IBD and non-IBD symptomatic children from healthy children, but displayed similar dysbiosis in IBD and non-IBD symptomatic patients. Pretreatment fecal microbiota profiles may be of prognostic value and aid in treatment individualization in pediatric IBD as severe dysbiosis was associated with an extensive, complicated phenotype, biologic therapy, and nonmucosal healing. The dysbiosis persisted after therapy, regardless of treatments and mucosal healing.


Crohn’s disease; Faecalibacterium prausnitzii; Proteobacteria; biologic therapy; dysbiosis; ulcerative colitis

Conflict of interest statement

Disclosure Christine Olbjørn is a member of the advisory board of AbbVie and has received speaker honoraria from AbbVie, Nutricia, Norgine, Tillotts Pharma, and Mead Johnson. Morten H Vatn has been an advisor for Genetic Analysis and organizer of the International Advisory Board of Genetic Analysis, a member of the advisory board for Tillotts Pharma, and has received speaker honoraria from AstraZeneca, AbbVie, MSD, and Falk. Gøri Perminow is a member of the advisory board of AbbVie and is a member of the steering committee in the IBSEN III study. The IBSEN III study has received an Investigator Initiated Research Grant from Takeda and nonrestricted research grants from Ferring Pharmaceuticals and Tillotts Pharma. Christina Casén and Magdalena K Karlsson are employed by Genetic Analysis. The authors report no other conflicts of interest in this work.

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