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Decline in Presumptively Protective Gut Bacterial Species and Metabolites Are Paradoxically Associated with Disease Improvement in Pediatric Crohn’s Disease During Enteral Nutrition

Gerasimidis, Konstantinos PhD*,†; Bertz, Martin MSc*,‡; Hanske, Laura PhD; Junick, Jana PhD; Biskou, Olga MSc*; Aguilera, Margarita PhD§; Garrick, Vikki BSc; Russell, Richard K. PhD*,†; Blaut, Michael PhD; McGrogan, Paraic PhD*,†; Edwards, Christine A. PhD*

doi: 10.1097/MIB.0000000000000023
Original Clinical Articles

Background: The gut microbiota is implicated in the pathogenesis of Crohn’s disease (CD). Exclusive enteral nutrition (EEN) is a successful treatment, but its mode of action remains unknown. This study assessed serial changes in the fecal microbiota milieu during EEN.

Methods: Five fecal samples were collected from CD children: 4 during EEN (start, 15, 30, end EEN approximately 60 days) and the fifth on habitual diet. Two samples were collected from healthy control subjects. Fecal pH, bacterial metabolites, global microbial diversity abundance, composition stability, and quantitative changes of total and 7 major bacterial groups previously implicated in CD were measured.

Results: Overall, 68 samples were from 15 CD children and 40 from 21 control subjects. Fecal pH and total sulfide increased and butyric acid decreased during EEN (all P < 0.05). Global bacterial diversity abundance decreased (P < 0.05); a higher degree of microbiota composition stability was seen in control subjects than in CD children during EEN (at P ≤ 0.008). Faecalibacterium prausnitzii spp concentration significantly decreased after 30 days on EEN (P < 0.05). In patients who responded to EEN, the magnitude of the observed changes was greater and the concentration of Bacteroides/Prevotella group decreased (P < 0.05). All these changes reverted to pretreatment levels on free diet, and EEN microbiota diversity increased when the children returned to their free diet.

Conclusions: EEN impacts on gut microbiota composition and changes fecal metabolic activity. It is difficult to infer a causative association between such changes and disease improvement, but the results do challenge the current perception of a protective role for F. prausnitzii in CD.

Article first published online 19 March 2014Supplemental Digital Content is Available in the Text.

*Human Nutrition, School of Medicine, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom;

Department of Pediatric Gastroenterology, Hepatology and Nutrition, National Health Service Scotland, Royal Hospital for Sick Children, Glasgow, United Kingdom;

Department of Gastrointestinal Microbiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Arthur-Scheunert-Allee, Nuthetal, Germany; and

§Department of Microbiology, Faculty of Pharmacy, University of Granada, Campus Universitario de Cartuja, Granada, Spain.

Reprints: Konstantinos Gerasimidis, PhD, Human Nutrition, School of Medicine, College of Medicine, Veterinary and Life Sciences, University of Glasgow, G3 8SJ, Glasgow, United Kingdom (e-mail:

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (

K. Gerasimidis received a postgraduate studentship by the Greek State Scholarship Foundation, the Hellenic Foundation of Gastroenterology, and Nutrition and the Barr Endowment Fund; a part of the running costs were funded by the Yorkhill Children’s Foundation. He also receives ongoing research grants from various charities. R. K. Russell has received support from a Medical Research Council patient research cohorts initiative grant (G0800675) for Paediatric Onset IBD Cohort and Treatment Study (PICTS) and is supported by an NHS Research Scotland career fellowship award. The IBD team at the Yorkhill Hospital, Glasgow, is supported by the Catherine McEwan Foundation and Yorkhill IBD fund. C. A. Edwards received grant from the Yorkhill Children’s Foundation and Crohn's in Childhood Research Association (CICRA). P. McGrogan received grant from the Yorkhill Children’s Foundation.

R. K. Russell has received speaker’s fees, travel support, and participated in medical board meetings with MSD Immunology, Abbott, Dr Falk, Nestle, and Ferring Pharmaceuticals. P. McGrogan received speaker fees, travel support, and participated in medical board meetings with Nestle, Falk, and MSD immunology. C. A. Edwards has participated in working groups for ILSI Europe and a workshop for Danone. She received consultancy fee from ILSI Europe and Foods Standards Agency and is employed with the University of Glasgow. V. Garrick received consultancy fee from Abbott and also payment for lectures from Warner Chillcott, MSD, Ferring, and Dr Falk. The other authors have no conflicts of interest to disclose.

Received January 16, 2014

Accepted February 02, 2014

© Crohn's & Colitis Foundation of America, Inc.
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