Kolho Kaija-Leena, Pessia Alberto, Jaakkola Tytti, de Vos Willem M, Velagapudi Vidya
Children's Hospital, Helsinki University Hospital, University of Helsinki, Helsinki, FIN-00029, Finland.
Metabolomics Unit, Institute for Molecular Medicine Finland FIMM, University of Helsinki, Helsinki, FIN-00029, Finland.
J Crohns Colitis. 2017 Mar 1;11(3):321-334. doi: 10.1093/ecco-jcc/jjw158.
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.
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.
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].
Characterization of inflammatory pattern using metabolomics analysis is a promising tool for better understanding disease pathogenesis of paediatric IBD.
炎症性肠病（IBD）被认为是宿主与肠道微生物群相互作用的结果，但其发病机制尚未完全明确。虽然成人IBD已显示与体液代谢组学的显著变化有关，但儿童相关研究较少。因此，这项前瞻性研究探讨了新诊断的儿童IBD患者的粪便和血清代谢组学。
在一家三级护理医院，患有IBD并接受诊断性内镜检查的儿科患者以及同样接受内镜检查但无炎症迹象的对照组提供了血液和粪便样本。测定了血液炎症标志物和粪便钙卫蛋白水平。使用超高压液相色谱-质谱联用仪测定血清和粪便代谢组学。
新诊断的儿童IBD患者的血清和粪便代谢物谱与健康对照不同，可将克罗恩病和溃疡性结肠炎（UC）患者分为不同组。在血清中，克罗恩病患者的氨基酸代谢、叶酸生物合成和信号通路受到干扰；与对照组相比，UC患者的鞘脂代谢途径也受到干扰。在粪便样本中，UC患者的几种代谢物水平升高，而克罗恩病患者的代谢物水平较低或中等。炎症水平与粪便钙卫蛋白水平以及各种重要生物代谢物（肌肽、核糖，最显著的是胆碱）的谱之间存在明显相关性。
利用代谢组学分析来表征炎症模式是更好地理解儿童IBD疾病发病机制的一个有前景的工具。
