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* = Presenting author

P713 Clinical remission induced by exclusive enteral nutrition (EEN) in pediatric Crohn's disease is associated with microbiome metabolic changes toward altered xenobiotic biodegradation and metabolism

J. Connors1, K.A. Dunn2, J.P. Bielawski2, A. Stadnyk3, N. Thomas4, A.R. Otley1, J. Van Limbergen*1, 4

1IWK Health Centre - Dalhousie University, Pediatric Gastroenterology & Nutrition, Halifax, Canada, 2Dalhousie University, Biology, Halifax, Canada, 3Dalhousie, Microbiology & Immunology, Halifax, Canada, 4Dalhousie University, Microbiology & Immunology, Halifax, Canada


Exclusive enteral nutrition (EEN) is a first-line induction therapy in pediatric Crohn's disease (CD). Though unclear, the mode of action of EEN is proposed to involve changes in gut microbiome structure and function. Characterization of the microbiome in IBD has largely focused on the assessment of diversity and the identification of protective and disease-associated species. More recently, metagenomic approaches to IBD microbiome investigation have facilitated predictive mapping of microbiome function. Treatment-induced changes to microbiome function may contribute to the strong therapeutic effect of EEN.

Our aims were to perform a functional assessment of microbial metabolic pathways in pediatric CD patients before and after induction of remission by EEN treatment.


Metagenomic sequences from stool samples obtained from 4 pediatric Crohn's disease patients who underwent EEN treatment were obtained using MiSeq whole-metagenome sequencing. Sequences were searched against 28 representative KEGG (Kyoto Kyoto Encyclopedia of Genes and Genomes) pathways to obtain functional assignment of sequences. Samples collected prior to EEN treatment were compared to samples collected after 8 to 12 weeks of EEN treatment. All participants achieved clinical remission (PCDAI <10) following EEN treatment.


Functional profiling of CD patient microbiota before and after EEN treatment revealed significant changes in metabolic functions related to biodegradation and metabolism of xenobiotics (e.g. benzoate), p<0.05.


The microbiome of CD patients is functionally altered by EEN treatment, specifically increasing metabolic potential for xenobiotic biodegradation and metabolism relative to pre-treatment. Further investigations of how altered xenobiotics metabolism contributes to the CD pathology and the therapeutic modality of EEN is warranted.