ArticleGut2025
Article in Gut, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- Identification of Gene Signatures and Molecular Mechanisms Underlying the Comorbidity of Alzheimer's Disease and Crohn's Disease Using Machine Learning.Psychiatry investigation · 2026Article
- Adhesion-Enhanced Engineered Probiotic for Prolonged Intestinal Retention and Calprotectin-Responsive IBD Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- From Multi-Omics to Molecular Causality: A Five-Tier Evidence Framework for the Single-Bacterium-Metabolite Axis in IBD.Microorganisms · 2026Review
- Watercress Extract Reduces Experimental Colitis by Modulating Inflammation and Regulating the Gut Microbiota.Nutrients · 2026Article
- Targeting tumor-associated bacteria in digestive system cancers: carcinogenic mechanisms and nano-regulate platform design.Journal of nanobiotechnology · 2026Review
- Plasma FABP2, IL-10, and LPS in Microscopic Colitis: An Exploratory Study of Their Biomarker Potential.Medicina (Kaunas, Lithuania) · 2026Article
- Engineered probiotics constitutively expressing SOD alleviate inflammatory bowel disease by targeting ROS.iScience · 2026Article
- Gut Lactate Boosts Ruminococcus via Histone Lactylation to Mediate Time-Restricted Feeding Protection in Crohn's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The role of the gut microbiota in radiation enteritis: from mechanistic insights to therapeutic applications.Communications biology · 2026Review
- Fatty acid-binding protein 2 in inflammatory bowel disease: mechanistic insights and translational perspectives.Frontiers in medicine · 2026Review
- Rewiring the Brain Through the Gut: Insights into Microbiota-Nervous System Interactions.Current issues in molecular biology · 2025Review
- "Envbiotics"-a concept based on host immune-gut environment and microbiota balance: expanding and refining the concepts of prebiotics and postbiotics.Frontiers in medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCrohn's disease (CD) is a chronic inflammatory disorder characterised by intestinal dysbiosis. While inflammation-induced leakage of host proteins is a known phenomenon in CD, how these proteins affect the gut microbiota and contribute to dysbiosis remains unclear. One hypothesis is that commensal bacteria hijack these proteins, exacerbating inflammation in CD.
designTo investigate host-microbiota interactions in CD, we measured fatty acid-binding protein 2 (FABP2) levels in patients with CD and in mouse models of dextran sulfate sodium induced enteritis and interleukin 10 knockout spontaneous enteritis. Proteomic approaches, including bacterial pull-down and mass spectrometry, were employed to identify commensal targets of FABP2. Functional studies were conducted using wild type and
resultsFABP2 levels were elevated in plasma and faeces of patients with CD, as well as in the mouse models. This was accompanied by dysbiosis of gut commensal bacteria.
conclusionThis study reveals a novel mechanism by which commensal bacteria use host-derived FABP2 to drive dysbiosis and worsen CD pathology. Targeting the FABP2-EF3041 axis may offer new diagnostic and therapeutic avenues for managing CD.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.