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From Microbiota to Metabolomics: How Bifidobacterium infantis YLGB-1496 Shields Neonates from Necrotizing enterocolitis

ABSTRACT:

Bifidobacterium species are recognized as essential primary colonizers of the infant gastrointestinal tract and constitute a critical component of infant formula. Nevertheless, the precise mechanisms by which Bifidobacterium confers its protective effects against gut inflammation remain insufficiently elucidated. In an experimental model of Necrotizing Enterocolitis (NEC), we observed that human milk-derived Bifidobacterium longum subsp. infantis YLGB-1496 (GB1496) demonstrated a significant protective effect against mortality, intestinal damage, and TLR-4-mediated inflammatory responses in neonatal mice. Subsequent analyses of the intestinal microbiota indicated that oral administration of GB1496 during the preventive phase markedly increased the abundance of Lactobacillus and Bifidobacterium. 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 further confirmed that elevated Bifidobacterium abundance facilitated the enhancement of tryptophan metabolism in the intestinal tract, which leaded to an overall increase in tryptophan metabolites. Collectively, our study suggested that GB1496 can prevent the occurrence of NEC by modulating the intestinal flora and flora-associated tryptophan metabolism in neonatal mice

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse phase, Liquid Chromatography MS - positive - reverse phase

PROVIDER: MTBLS13018 | MetaboLights | 2025-10-20

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS13018_LC-MS_negative_reverse-phase_metabolite_profiling.txt	Txt
	a_MTBLS13018_LC-MS_positive_reverse-phase_metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS13018_LC-MS_negative_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular
	m_MTBLS13018_LC-MS_positive_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular

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Project description:<p>The intestinal microflora and metabolites produced by these microbes serve as important regulators of the development of sepsis. Accordingly, this study was designed to systematically explore the relationships between the regulation of septicemia and both the intestinal flora and fecal metabolites by examining the functional roles of metabolites in the protection against sepsis-associated intestinal damage. To that end, fecal and peripheral blood mononuclear cell (PBMC) samples were collected from sepsis patients and healthy controls. A series of longitudinal multi-omics analyses were then used to assess the links between the intestinal flora or associated metabolites and PBMCs in sepsis patients, while animal model studies were further used to probe the protective effects of intestinal flora-derived metabolites on intestinal damage and immunity in the context of sepsis. These analyses revealed that intestinal dysbiosis was a common finding in sepsis patients, which commonly exhibited higher levels of deleterious bacteria and/or reductions in beneficial bacteria. A machine learning approach was used to identify samples from sepsis patients, revealing that at the genus level, sepsis samples could be distinguished by the presence of Bifidobacterium, Bacteroides, Porphyromonas, Prevotell, Enterococcus, Anaerococcus and Veillonella species. Metabolomics analyses indicated that there were significant differences in the levels of intestinal flora-derived metabolites including L-serine, L-valine and L-tyrosine when comparing samples from the sepsis and control groups, while corresponding transcriptomic analyses of PBMC samples using an ImmunecellAI analytical approach revealed a significant sepsis-related increase in the abundance of T cells and Th17 cells. Single-cell sequencing data from sepsis-associated PBMCs was also downloaded from the GEO database, confirming the observation that Th17 cell levels and those of other immune cells rose significantly in the context of septicemia. Animal model experiments revealed that intestinal microbiota-derived L-valine was able to alleviate inflammation and protest against sepsis-induced intestinal damage by inhibiting Th17 cell activation. Overall, these results thus highlight the successful application of machine learning to distinguish between sepsis and control samples based on the composition of the intestinal flora while demonstrating the potential therapeutic benefits of L-valine as an inhibitor of Th17 cell activity that may offer value as a means of alleviating or preventing intestinal damage in treated individuals. </p>

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From Microbiota to Metabolomics: How Bifidobacterium infantis YLGB-1496 Shields Neonates from Necrotizing enterocolitis

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