Infant gut microbiome development is strongly impacted by breastmilk and human milk oligosaccharides (HMOs), which can protect preterm infants against pathologies including necrotising enterocolitis. HMO metabolism in bifidobacteria is well-characterised and linked to health outcomes, but the scope of HMO-utilising species remains unclear. Here, using a combination of genomics, proteomics, and metabolomics, we show that Clostridium species isolated from preterm infants (born <32 weeks’ gestation), in particular Clostridium perfringens lacking the toxin perfringolysin O (PfoA), metabolised 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 metabolising microbes and suggest that pfoA- C. perfringens strains could contribute to healthy infant gut development.