ArticleNature microbiology2026
Clostridia from preterm infants metabolize human milk oligosaccharides to suppress pathobionts and modulate intestinal function in organoids.
Article in Nature microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
The trial behind it
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Who cites it
5 citing papers in PubMed.
- Nationwide cohort study reveals low bifidobacteria and distinct microbiota composition and function in Swedish newborns.Gut microbes · 2026Observational
- Early microbial encounters, lasting effects: strains matter.Nature reviews. Microbiology · 2026Article
- Early Gut Microbiota and Metabolic Profiles of Neonatal Donkey Foals and a Comparative Study with Maternal Communities.Microorganisms · 2026Article
- Fatal Acute Thyroiditis in a Giraffe (Animals : an open access journal from MDPI · 2026Article
- Human milk oligosaccharide mediates mutualism between Escherichia coli and Bifidobacterium bifidum.Nature communications · 2026Article
Corrections and comments
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Authors and funding
21 authors.
Funding
Abstract
Infant gut microbiome development is strongly impacted by breastmilk and human milk oligosaccharides (HMOs), which can protect preterm infants against pathologies including necrotizing enterocolitis. HMO metabolism in bifidobacteria is well characterized and linked to health outcomes, but the scope of HMO-utilizing species remains unclear. Here, using a combination of genomics, proteomics and metabolomics, we show that Clostridium species isolated from preterm infants (born at <32 weeks gestation), in particular Clostridium perfringens lacking the toxin perfringolysin O (PfoA), metabolized HMOs. Clostridium species produced beneficial metabolites including short-chain fatty acids and tryptophan catabolites at higher quantities than Bifidobacterium species in vitro. Cell-free supernatant from C. perfringens was non-toxic to colonic cell lines, promoted the growth of commensal bifidobacteria and inhibited growth of pathobionts isolated from the preterm infant gut in vitro. It also suppressed inflammation in preterm-derived intestinal organoids. These findings expand our understanding of HMO-metabolizing microbes and suggest that pfoA
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Registered trials
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