ArticleCell reports. Medicine2026
Early-life immune imprinting by a B. infantis-HMO synbiotic shapes infant immune signatures and protects against experimental respiratory disease.
Article in Cell reports. Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Early microbial colonization influences immune development, with lower abundance of human milk oligosaccharide (HMO)-utilizing bifidobacteria linked to immune-related disorder risk. Here, we demonstrate that synbiotic supplementation with Bifidobacterium infantis (LMG 11588) and a blend of six structurally diverse HMOs plus Bifidobacterium lactis (CNCM I-3446) altered gut microbiome composition, changed systemic immune cell-networks, and reduced persistence of a T helper 2 (Th2) bias in formula-fed infants, following a pattern observed in breastfed infants. In preclinical models, synbiotic reduces lower respiratory tract infection (LRI) severity and aberrant type-2 immune responses and confers lasting immune benefits into adulthood. These effects are associated with changes in the circulating metabolome, including increased 12(S)-hydroxyheptadecatrienoic acid (12-HHT), which correlates with improved infection outcomes and phenocopies synbiotic-mediated protection when administered orally. Together, these findings indicate that infant-type synbiotic supplementation during a critical early-life window can imprint immune function and promote disease tolerance.
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