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<p>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 <i>Clostridium</i> species isolated from preterm infants (born at &lt;32 weeks gestation), in particular <i>Clostridium perfringens</i> lacking the toxin perfringolysin O (PfoA), metabolized HMOs. <i>Clostridium</i> species produced beneficial metabolites including short-chain fatty acids and tryptophan catabolites at higher quantities than <i>Bifidobacterium</i> species in vitro. Cell-free supernatant from <i>C. perfringens</i> 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 <i>pfoA</i><sup><i>−</i></sup> <i>C. perfringens</i> strains could contribute to healthy infant gut development.</p>

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Clostridia from preterm infants metabolize human milk oligosaccharides to suppress pathobionts and modulate intestinal function in organoids

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月16日

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  • Jonathan A. Chapman,
  • Andrea C. Masi,
  • Lauren C. Beck,
  • Hannah Watson,
  • Gregory R. Young,
  • Hilary P. Browne,
  • Yan Shao,
  • Raymond Kiu,
  • Andrew Nelson,
  • Jennifer A. Doyle,
  • Pawel Palmowski,
  • Márton Lengyel,
  • James P. R. Connolly,
  • Christopher A. Lamb,
  • Andrew Porter,
  • Trevor D. Lawley,
  • Lindsay J. Hall,
  • Nicholas D. Embleton,
  • John D. Perry,
  • Janet E. Berrington,
  • Christopher J. Stewart

摘要

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− C. perfringens strains could contribute to healthy infant gut development.