Mo1814 The N- Acyl-Homoserine Lactone 3-oxo-C12, an Inter-Bacterial Signaling Molecule (Involved in Quorum Sensing), Exerts Effects on the Host: Thus Implicating Quorum Sensing in Inflammatory Bowel Disease

Abstract

Background 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 compare microbial community structure and functional assessments of microbial metabolic pathways in pediatric CD patients before and after induction of remission by EEN treatment. Methods 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 the SILVA database to obtain microbial composition profiles based on 16S ribosomal RNA genes. To obtain functional assignment, sequences were searched against 28 representative KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways. 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. Results Changes in CD patient microbial community structure before and after EEN were variable. However, functional profiling of CD patient microbiota before and after EEN treatment revealed a significant increase in metabolic functions related to biodegradation and metabolism of xenobiotics, such as benzoate (p<0.05). Conclusions 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 are warranted to investigate the role of altered xenobiotics metabolism in the therapeutic modality of EEN, as well as CD etiopathogenesis.