ArticleNutrients2024
Exploring the Immunomodulatory Potential of Human Milk: Aryl Hydrocarbon Receptor Activation and Its Impact on Neonatal Gut Health.
Article in Nutrients, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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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Who cites it
7 citing papers in PubMed.
- Six-compound cocktail for maturation of human pluripotent stem cell-derived liver spheroids for toxicity prediction.Nature communications · 2026Article
- Mechanisms by which tryptophan metabolites enhance intestinal barrier function to prevent necrotizing enterocolitis in preterm infants.Frontiers in immunology · 2026Review
- Longitudinal analysis of fecal tryptophan metabolites and microbiome composition in very preterm infants: impact of birth mode and feeding type.Gut microbes · 2025Article
- Aryl Hydrocarbon Receptor in Health and Disease.MedComm · 2025Review
- Indole-3-lactic acid protects the gut vascular barrier following intestinal ischemia injury through AhR/Nrf2/STAT3 mediated claudin 2 downregulation.Cell communication and signaling : CCS · 2025Article
- Mechanisms and Therapeutic Potential of Key Anti-inflammatory Metabiotics: Trans-Vaccenic Acid, Indole-3-Lactic Acid, Thiamine, and Butyric Acid.Probiotics and antimicrobial proteins · 2025Review
- Article
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Authors and funding
13 authors.
Funding
Abstract
Several metabolites of the essential amino acid tryptophan have emerged as key players in gut homeostasis through different cellular pathways, particularly through metabolites which can activate the aryl hydrocarbon receptor (AHR). This study aimed to map the metabolism of tryptophan in early life and investigate the effects of specific metabolites on epithelial cells and barrier integrity. Twenty-one tryptophan metabolites were measured in the feces of full-term and preterm neonates as well as in human milk and formula. The ability of specific AHR metabolites to regulate cytokine-induced IL8 expression and maintain barrier integrity was assessed in Caco2 cells and human fetal organoids (HFOs). Overall, higher concentrations of tryptophan metabolites were measured in the feces of full-term neonates compared to those of preterm ones. Within AHR metabolites, indole-3-lactic acid (ILA) was significantly higher in the feces of full-term neonates. Human milk contained different levels of several tryptophan metabolites compared to formula. Particularly, within the AHR metabolites, indole-3-sulfate (I3S) and indole-3-acetic acid (IAA) were significantly higher compared to formula. Fecal-derived ILA and milk-derived IAA were capable of reducing TNFα-induced IL8 expression in Caco2 cells and HFOs in an AHR-dependent manner. Furthermore, fecal-derived ILA and milk-derived IAA significantly reduced TNFα-induced barrier disruption in HFOs.
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Registered trials
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