Abstract
Inflammatory bowel disease is a multifactorial etiology, associated with environmental factors that can trigger both debut and relapses. A high level of tumor necrosis factor-α in the gut is the main consequence of immune system imbalance. The aim of treatment is to restore gut homeostasis. In this study, fresh blood and serum samples were used to identify biomarkers and to discriminate between Crohn’s disease and ulcerative colitis patients under remission treated with anti-TNF. Metabolomics based on Nuclear Magnetic Resonance spectroscopy (NMR) was used to detect unique biomarkers for each class of patients. Blood T lymphocyte repertories were characterized, as well as cytokine and transcription factor profiling, to complement the metabolomics data. Higher levels of homoserine-methionine and isobutyrate were identified as biomarkers of Crohn’s disease with ileocolic localization. For ulcerative colitis, lower levels of creatine-creatinine, proline, and tryptophan were found that reflect a deficit in the absorption of essential amino acids in the gut. T lymphocyte phenotyping and its functional profiling revealed that the overall inflammation was lower in Crohn’s disease patients than in those with ulcerative colitis. These results demonstrated that NMR metabolomics could be introduced as a high-throughput evaluation method in routine clinical practice to stratify both types of patients related to their pathology.Key messagesNMR metabolomics is a non-invasive tool that could be implemented in the normal clinical practice for IBD to assess beneficial effect of the treatment.NMR metabolomics is a useful tool for precision medicine, in order to sew a specific treatment to a specific group of patients.Finding predictors of response to IFX would be desirable to select patients affected by IBD.Immunological status of inflammations correlates with NMR metabolomics biomarkers.
Highlights
Inflammatory bowel disease (IBD) is a chronic intestinal inflammatory condition, of unidentified etiology, that comprises two major distinct pathologies: Crohn’s disease (CD) and ulcerative colitis (UC); CD can affect both the ileum and colon while UC is limited to the colon
Antigen-presenting cells (APC), such as dendritic cells (DC) or intestinal epithelial cells, are able to sense the extra-luminal environment and cooperate with the gut adaptive immune system to maintain a tolerogenic response by activation of the CD4+ T regulatory subset, expressing forkhead box P3 (FoxP3) transcription factor, and thereby secreting interleukin-10 into the gut lamina propria
Patients were divided into two groups according to the Montreal classification: Crohn disease (CD, n = 18, divided into 3 subgroups depending on the disease localization in ILEUM, n = 8; COLON, n = 4; and ILEOCOLIC, n = 6) and Ulcerative colitis (UC, n = 9) with average age of 45 years from 19 to 69, and equal sex representation
Summary
Inflammatory bowel disease (IBD) is a chronic intestinal inflammatory condition, of unidentified etiology, that comprises two major distinct pathologies: Crohn’s disease (CD) and ulcerative colitis (UC); CD can affect both the ileum and colon while UC is limited to the colon. Aberrant T cell activation and proliferation are one of the mechanisms responsible for IBD, where high amounts of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-17 (IL-17), or interferon-γ (IFN-γ) are released in the gut epithelium by activated Th1, or Th17 [3]. It is not clear if microbiota translocations are the cause or the effect of aberrant inflammation since both the high levels of TNF-α and Th1 over activation determine aberrant proliferation and autoimmunity
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