ArticleAnimal bioscience2026
Gut microbiota-derived tryptophan metabolite indole-3-carboxaldehyde enhances intestinal barrier function via aryl hydrocarbon receptor/AMP-activated protein kinase signaling activation.
Article in Animal bioscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Microbiome-Derived Tryptophan Metabolites Regulate AhR Signaling to Restore Epithelial Barrier Integrity in Inflammatory Bowel Disease.MicrobiologyOpen · 2026Review
- Limosilactobacillus reuteri orchestrates IAA-mediated mitochondrial homeostasis and stem cell renewal against intestinal oxidative injury in aged hens.Journal of animal science and biotechnology · 2026Article
- Bifidobacterium modulates gut microbiota and aryl hydrocarbon receptor signaling in necrotizing enterocolitis rat model.Pediatric research · 2026Article
- Dietary Regulation of Intestinal Stem Cell Function: Nutrient-Sensing, Microbiota-Mediated, and Regenerative Mechanisms from a Dietetic Perspective.Biomedicines · 2026Review
- Review
- Indole-3-Propionic Acid Alleviates Metabolic Dysfunction-Associated Fatty Liver Disease via AHR/AMPK Signaling Activation.Food science & nutrition · 2026Article
- Postbiotic Nagqu4580 Attenuates Ulcerative Colitis and Suppresses Ferroptosis in Association with the Microbiota-Tryptophan-AhR/Nrf2 Axis.Nutrients · 2026Article
- Gut microbiota and aging: current understanding and future perspectives.Molecular biomedicine · 2026Review
- Aryl hydrocarbon receptor regulates programmed cell death in diseases: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
objectiveIntestinal inflammatory diseases significantly affect animal health, primarily by disrupting intestinal barrier function. Indole-3-carboxaldehyde (IAld), a key metabolite of tryptophan derived from gut microbiota, exhibits protective properties against intestinal inflammatory diseases. The regulatory mechanism by which IAld modulates intestinal barrier function requires further investigation.
methodsAn intestinal epithelial cell injury model was established by tumor necrosis factor-alpha (TNF-α) stimulation, alongside a mouse colitis model induced by dextran sulfate sodium (DSS) administration. Intestinal barrier function was assessed by immunoblotting, immunofluorescence, in vitro permeability assays, and histopathological analysis. Mitochondrial integrity and function were evaluated using JC-1 staining and transmission electron microscopy. Additionally, key components of the aryl hydrocarbon receptor (AhR)/AMP-activated protein kinase (AMPK) signaling pathway were analyzed using immunoblotting, immunofluorescence, and immunoprecipitation techniques.
resultsOur findings demonstrate that IAld treatment significantly enhanced tight junction protein expression in intestinal epithelial cells and effectively attenuated TNF-α-induced intestinal barrier injury. IAld activated cellular AMPK signaling, promoting autophagy, maintaining mitochondrial homeostasis, and ultimately improving intestinal barrier function. Importantly, the activation of AMPK signaling by IAld was found to be dependent on the AhR, as evidenced by the AhR-specific inhibitor CH-223191, which abolished both IAld-induced AMPK activation and enhancement of intestinal barrier integrity. Furthermore, in vivo< experiments confirmed that IAld ameliorated intestinal barrier dysfunction and mitochondrial damage in DSS-induced colitis mice, whereas pharmacological inhibition of AMPK largely abrogated these protective effects.
conclusionOur findings demonstrate that IAld effectively preserves intestinal barrier integrity, highlighting its potential application in the treatment of intestinal inflammatory diseases in both animals and humans.
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