Biotin Supplementation Ameliorates Murine Colitis by Preventing NF-κB ActivationSummary
| Autor: | Hamid M. Said, Jonathan Skupsky, Michael D. Cahalan, Manando Nakasaki, Subrata Sabui, Michael Hwang |
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| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Crohn's Disease Pharmacology Inbred C57BL Inflammatory bowel disease Oral and gastrointestinal DAI Disease Activity Index Mice chemistry.chemical_compound PCR polymerase chain reaction 0302 clinical medicine Biotin 2.1 Biological and endogenous factors DSS dextran sodium sulfate Micronutrients Aetiology Cancer Original Research TNF tumor necrosis factor IBD inflammatory bowel disease Stem Cells Dextran Sulfate NF-kappa B Gastroenterology ELISA enzyme-linked immunosorbent assay SMVT sodium-dependent multivitamin transporter GI gastrointestinal Colitis Colo-Rectal Cancer 3. Good health Editorial 030211 gastroenterology & hepatology Tumor necrosis factor alpha FITC fluorescein isothiocyanate Signal Transduction Kruppel-Like Transcription Factors NF-κB nuclear factor-κB Biotin deficiency Therapeutics Autoimmune Disease Proinflammatory cytokine 03 medical and health sciences medicine Humans Regeneration Animals lcsh:RC799-869 Nutrition Intestinal permeability Hepatology business.industry Inflammatory Bowel Disease Inflammatory Bowel Diseases medicine.disease IL interleukin Mice Inbred C57BL UC ulcerative colitis 030104 developmental biology chemistry Dietary Supplements lcsh:Diseases of the digestive system. Gastroenterology Calprotectin Digestive Diseases business |
| Zdroj: | Cellular and Molecular Gastroenterology and Hepatology, Vol 9, Iss 4, Pp 557-567 (2020) Cellular and Molecular Gastroenterology and Hepatology Cellular and molecular gastroenterology and hepatology, vol 9, iss 4 |
| Popis: | Background & Aims Biotin is a water-soluble vitamin that is indispensable for human health. Biotin deficiency can cause failure-to-thrive, immunodeficiency, alopecia, dermatitis, and conjunctivitis. We previously reported that biotin deficiency also can lead to severe colitis in mice, which is completely reversed with supplementation. Our aim in this study was to determine if high-dose biotin supplementation can provide a therapeutic benefit in a preclinical model for inflammatory bowel disease (IBD) and to identify the molecular mechanism by which this occurs. Methods Mice were challenged with dextran sodium sulfate to induce colitis and were treated with 1 mmol/L biotin to induce or maintain remission. Clinical response was monitored by the Disease Activity Index and fecal calprotectin levels. The colon tissue was investigated for histology, length, as well as expression of inflammatory cytokines (interleukin 6, tumor necrosis factor-α, interleukin 1β), intestinal permeability, tight junctions (zonula occludens-1 and claudin-2), and the transcription factor nuclear factor-κB (NF-κB). Results Biotin therapy led to delayed onset and severity of colitis as well as accelerated healing. There was improvement in the Disease Activity Index, fecal calprotectin levels, colon length, and histology. In addition, biotin-treated mice had reduced expression of inflammatory cytokines, reduced intestinal permeability, and reduced activation of NF-κB. Conclusions Oral supplementation with biotin provides benefit for maintenance and induction of remission in the dextran sodium sulfate preclinical model for IBD. Biotin does this by reducing the activation of NF-κB, which prevents the production of inflammatory cytokines and helps maintain the integrity of the intestinal barrier. Clinically, the NF-κB pathway is important in the development of IBD and this finding suggests that biotin may have therapeutic potential for patients with IBD. Graphical abstract |
| Databáze: | OpenAIRE |
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