Milk-derived tripeptide enriches Dubosiella newyorkensis and elicits Aryl hydrocarbon receptor activation to ameliorate colitis through ferroptosis inhibition
This dataset corresponds to the study exploring the protective mechanism of milk-derived bioactive tripeptide Val-Pro-Pro (VPP) against dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice. The experiments included 16S rRNA gene sequencing of mouse fecal microbiota and metabolomic profiling of intestinal contents to characterize gut microbial community shifts and metabolite alterations after VPP intervention. Specifically, we analyzed the enrichment of Dubosiella newyorkensis and the production of its tryptophan metabolite 5-methoxy-2-methylindole-3-acetic acid (MMIA) in VPP-treated mice. Additionally, transcriptomic data of intestinal epithelial cells were generated to verify the downregulation of iron uptake-related genes (DMT1, DCYTB) and the activation of the aryl hydrocarbon receptor (AHR) pathway, as well as the subsequent inhibition of ferroptosis. Pharmacological and genetic inhibition experiments targeting AHR were also performed to confirm the critical role of the D. newyorkensis-MMIA-AHR-ferroptosis axis in VPP-mediated anti-colitis activity. These data provide a comprehensive resource for investigating the interplay between milk bioactive peptides, gut microbiota, and host immune-metabolic homeostasis in UC pathogenesis and treatment.