ArticleCellular and molecular gastroenterology and hepatology2021
Enterococcus faecalis Glucosamine Metabolism Exacerbates Experimental Colitis.
Article in Cellular and molecular gastroenterology and hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- An atlas of colonization factors in the human gut microbiome reveals ecological strategies and inflammatory bowel disease signatures.Nature communications · 2026Article
- Effect of a Polysaccharide from CultivatedNutrients · 2026Article
- Targeting the Gut Microbiota with Herbal Compounds from Traditional Chinese Medicine: A Mechanistic Synthesis of a Novel Therapeutic Approach for Ulcerative Colitis.Journal of inflammation research · 2026Review
- Gut microbiota in regulatory T cell generation and function: mechanisms and health implications.Gut microbes · 2025Review
- Enterococcus proliferates via the phosphotransferase system in the disrupted gut microbiota after allogeneic haematopoietic stem cell transplantation.British journal of haematology · 2025Article
- The Role of Gut Microbiota in Gastrointestinal Immune Homeostasis and Inflammation: Implications for Inflammatory Bowel Disease.Biomedicines · 2025Review
- Changes in amino acid concentrations and the gut microbiota composition are implicated in the mucosal healing of ulcerative colitis and can be used as noninvasive diagnostic biomarkers.Clinical proteomics · 2024Article
- An olsalazine nanoneedle-embedded inulin hydrogel reshapes intestinal homeostasis in inflammatory bowel disease.Bioactive materials · 2024Article
- Integrative Multiomics Profiling Unveils the Protective Function of Ulinastatin against Dextran Sulfate Sodium-Induced Colitis.Antioxidants (Basel, Switzerland) · 2024Article
- Celery soluble dietary fiber antagonizes flavonoids ameliorative effect on dextran-sodium-sulfate-induced colitis in mice.Journal of advanced research · 2023Article
- Genetic characterization of MDR genomic elements carrying twoFrontiers in microbiology · 2023Article
- Different Effects of DifferentInternational journal of molecular sciences · 2022Article
- When Pathobiont-Carbohydrate Interaction Turns Bittersweet!Cellular and molecular gastroenterology and hepatology · 2021Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsThe inflammatory bowel diseases (IBDs), Crohn's disease and ulcerative colitis, are caused in part by aberrant immune responses to resident intestinal bacteria. Certain dietary components, including carbohydrates, are associated with IBDs and alter intestinal bacterial composition. However, the effects of luminal carbohydrates on the composition and colitogenic potential of intestinal bacteria are incompletely understood. We hypothesize that carbohydrate metabolism by resident proinflammatory intestinal bacteria enhances their growth and worsens intestinal inflammation.
methodsWe colonized germ-free, wild-type, and colitis-susceptible interleukin-10 knockout mice (Il10
resultsWe show that a consortium of 8 bacterial strains induces severe colitis in Il10
conclusionsFurther studies of luminal carbohydrate levels and bacterial carbohydrate metabolism during intestinal inflammation will improve our understanding of the pathogenesis of IBDs and may lead to the development of novel therapies for these diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.