Kaija-Leena Kolho1, Alberto Pessia2, Tytti Jaakkola1, Willem M de Vos3,4,5, Vidya Velagapudi2. 1. Children's Hospital, Helsinki University Hospital, University of Helsinki, Helsinki, FIN-00029, Finland. 2. Metabolomics Unit, Institute for Molecular Medicine Finland FIMM, University of Helsinki, Helsinki, FIN-00029, Finland. 3. Immunobiology Program, Department of Bacteriology & Immunology, University of Helsinki, Helsinki, FIN-00029, Finland. 4. Laboratory of Microbiology, Wageningen University, 6703 HB Wageningen, The Netherlands. 5. Department of Veterinary Biosciences, University of Helsinki, Helsinki, FIN-00029, Finland.
Abstract
BACKGROUND: Inflammatory bowel disease [IBD] is considered to result from the interplay between host and intestinal microbiota but its pathogenesis is incompletely understood. While IBD in adults has shown to be associated with marked changes in body fluid metabolomics, there are only few studies in children. Hence, this prospective study addressed the faecal and serum metabolomics in newly diagnosed paediatric IBD. METHODS: Paediatric patients with IBD undergoing diagnostic endoscopies and controls also with endoscopy but no signs of inflammation provided blood and stool samples in a tertiary care hospital. Blood inflammatory markers and faecal calprotectin levels were determined. The serum and faecal metabolomics were determined using ultra-high pressure liquid chromatography coupled to a mass spectrometer. RESULTS: Serum and faecal metabolite profiles in newly diagnosed paediatric IBD patients were different from healthy controls and categorized Crohn's disease and ulcerative colitis [UC] patients into separate groups. In serum, amino acid metabolism, folate biosynthesis and signalling pathways were perturbed in Crohn's disease; in UC also sphingolipid metabolic pathways were perturbed when compared to controls. In faecal samples, there was an increased level of several metabolites in UC in contrast to low or intermediate levels in Crohn's disease. There was a clear correlation with the level of inflammation, i.e. faecal calprotectin levels and the profile of various biologically important metabolites [carnosine, ribose and, most significantly, choline]. CONCLUSION: Characterization of inflammatory pattern using metabolomics analysis is a promising tool for better understanding disease pathogenesis of paediatric IBD.
BACKGROUND: Inflammatory bowel disease [IBD] is considered to result from the interplay between host and intestinal microbiota but its pathogenesis is incompletely understood. While IBD in adults has shown to be associated with marked changes in body fluid metabolomics, there are only few studies in children. Hence, this prospective study addressed the faecal and serum metabolomics in newly diagnosed paediatric IBD. METHODS: Paediatric patients with IBD undergoing diagnostic endoscopies and controls also with endoscopy but no signs of inflammation provided blood and stool samples in a tertiary care hospital. Blood inflammatory markers and faecal calprotectin levels were determined. The serum and faecal metabolomics were determined using ultra-high pressure liquid chromatography coupled to a mass spectrometer. RESULTS: Serum and faecal metabolite profiles in newly diagnosed paediatric IBD patients were different from healthy controls and categorized Crohn's disease and ulcerative colitis [UC] patients into separate groups. In serum, amino acid metabolism, folate biosynthesis and signalling pathways were perturbed in Crohn's disease; in UC also sphingolipid metabolic pathways were perturbed when compared to controls. In faecal samples, there was an increased level of several metabolites in UC in contrast to low or intermediate levels in Crohn's disease. There was a clear correlation with the level of inflammation, i.e. faecal calprotectin levels and the profile of various biologically important metabolites [carnosine, ribose and, most significantly, choline]. CONCLUSION: Characterization of inflammatory pattern using metabolomics analysis is a promising tool for better understanding disease pathogenesis of paediatric IBD.
Authors: Elizabeth A Scoville; Margaret M Allaman; Caroline T Brown; Amy K Motley; Sara N Horst; Christopher S Williams; Tatsuki Koyama; Zhiguo Zhao; Dawn W Adams; Dawn B Beaulieu; David A Schwartz; Keith T Wilson; Lori A Coburn Journal: Metabolomics Date: 2017-12-29 Impact factor: 4.290
Authors: Frederic D Bushman; Maire Conrad; Yue Ren; Chunyu Zhao; Christopher Gu; Christopher Petucci; Min-Soo Kim; Arwa Abbas; Kevin J Downes; Nina Devas; Lisa M Mattei; Jessica Breton; Judith Kelsen; Sarah Marakos; Alissa Galgano; Kelly Kachelries; Jessi Erlichman; Jessica L Hart; Michael Moraskie; Dorothy Kim; Huanjia Zhang; Casey E Hofstaedter; Gary D Wu; James D Lewis; Joseph P Zackular; Hongzhe Li; Kyle Bittinger; Robert Baldassano Journal: Cell Host Microbe Date: 2020-08-20 Impact factor: 31.316