From microbiota to metabolomics: how Bifidobacterium infantis YLGB-1496 shields neonates from necrotizing enterocolitis

. Furthermore, serum untargeted metabolomics revealed significant alterations in the levels of tryptophan metabolites. Specific tryptophan metabolites, such as indole-3-acetic acid, L-formylkynurenine, and 5-hydroxyindole-3-acetic acid, were significantly enriched following GB1496 intervention, potentially activating the AHR-associated anti-inflammatory pathway as ligands. Correlation analysis indicates a potential association between GB1496-induced Bifidobacterium enrichment and enhanced intestinal tryptophan metabolism. The collective impact of GB1496 intervention has been demonstrated to engender an augmentation in Bifidobacterium abundance, a concomitant downregulation of inflammatory factors associated with the TLR-4 pathway, and an induction of alterations in serum tryptophan metabolites. It is evident that these combined effects contribute to its protective action against NEC.