Bifidobacteria are specifically capable of metabolising 2’-FL, due to their expression of adequate transporters and intracellular enzyme machinery12,20. On the contrary, pathogens, such as E. coli or Clostridium prefringens cannot metabolise 2’-FL12. So the presence of 2’-FL gives the bifidobacteria a competitive advantage for growth in the gut.
Using infant fecal slurries to represent the intestinal microbial communities, supplementation with HMOs was found to significantly increase the number of bifidobacteria, with decreases in the number of Escherichia spp. and Clostridium perfringens.12 This study also showed that over 90% of the 2’-FL and lactodifucotetraose (LDFT), and 53% of 3-FL, from the supplemental HMO was consumed by the cultured fecal microbiota, supporting the hypothesis that some oligosaccharides have stronger prebiotic effects than others. Upon testing the responses of individual bacteria to supplementation with three major individual oligosaccharides (2’-FL, 3-FL and LDFT), it was shown that, when cultured with Bifidobacterium longum JCM7007 and B. longum ATCC15697, all three exhibit key characteristics of a prebiotic in vitro. In vitro studies have shown that beneficial bifidobacteria are specifically capable of metabolising 2’-FL, due to their expression of adequate transporters and intracellular enzyme machinery.20,28 Bifidobacterium species are very early colonizers in breastfed infants, with select, common species able to use HMOs as metabolic substrates.28 in infants breastfed by secretor mothers, bifidobacteria were established earlier, and a higher proportion of bifidobacteria isolated from infants fed by secretor mothers were shown to consume 2’-FL, compared with infants fed milk from non-secretor mothers.28 These results suggest that 2’-fucosylated oligosaccharides, among which 2’-FL, drive colonization of the infant gut with bifidobacteria.