Faecal and Serum Metabolomics in Paediatric Inflammatory Bowel Disease.
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].


CONCLUSIONS
Characterization of inflammatory pattern using metabolomics analysis is a promising tool for better understanding disease pathogenesis of paediatric IBD.
Children's Hospital, Helsinki University Hospital, University of Helsinki, Helsinki, FIN-00029, Finland.
Kaija-Leena
KL
Kolho
Metabolomics Unit, Institute for Molecular Medicine Finland FIMM, University of Helsinki, Helsinki, FIN-00029, Finland.
Alberto
A
Pessia
Children's Hospital, Helsinki University Hospital, University of Helsinki, Helsinki, FIN-00029, Finland.
Tytti
T
Jaakkola
Immunobiology Program, Department of Bacteriology & Immunology, University of Helsinki, Helsinki, FIN-00029, Finland.|Laboratory of Microbiology, Wageningen University, 6703 HB Wageningen, The Netherlands.|Department of Veterinary Biosciences, University of Helsinki, Helsinki, FIN-00029, Finland.
Willem M
WM
de Vos
Metabolomics Unit, Institute for Molecular Medicine Finland FIMM, University of Helsinki, Helsinki, FIN-00029, Finland.
Vidya
V
Velagapudi
D000293:Adolescent; D000596:Amino Acids / Q000097:blood; D002336:Carnosine / Q000032:analysis; D016022:Case-Control Studies; D002648:Child; D002794:Choline / Q000032:analysis; D003093:Colitis, Ulcerative / Q000097:blood* / Q000378:metabolism; D003424:Crohn Disease / Q000097:blood* / Q000378:metabolism; D005243:Feces / Q000737:chemistry*; D005260:Female; D005492:Folic Acid / Q000096:biosynthesis; D006801:Humans; D039841:Leukocyte L1 Antigen Complex / Q000032:analysis; D008297:Male; D053858:Metabolic Networks and Pathways; D055432:Metabolomics; D011446:Prospective Studies; D012266:Ribose / Q000032:analysis; D012737:Sex Factors; D015398:Signal Transduction; D013107:Sphingolipids / Q000378:metabolism
D000596:Amino Acids; D039841:Leukocyte L1 Antigen Complex; D013107:Sphingolipids; D012266:Ribose; D002336:Carnosine; D005492:Folic Acid; D002794:Choline
Children; Crohn’s disease; ulcerative colitis