Abstract
BackgroundIndividuals with inactive alleles of the fucosyltransferase 2 gene (FUT2; termed the ‘secretor’ gene) are common in many populations. Some members of the genus Bifidobacterium, common infant gut commensals, are known to consume 2′-fucosylated glycans found in the breast milk of secretor mothers. We investigated the effects of maternal secretor status on the developing infant microbiota with a special emphasis on bifidobacterial species abundance.ResultsOn average, bifidobacteria were established earlier and more often in infants fed by secretor mothers than in infants fed by non-secretor mothers. In secretor-fed infants, the relative abundance of the Bifidobacterium longum group was most strongly correlated with high percentages of the order Bifidobacteriales. Conversely, in non-secretor-fed infants, Bifidobacterium breve was positively correlated with Bifidobacteriales, while the B. longum group was negatively correlated. A higher percentage of bifidobacteria isolated from secretor-fed infants consumed 2′-fucosyllactose. Infant feces with high levels of bifidobacteria had lower milk oligosaccharide levels in the feces and higher amounts of lactate. Furthermore, feces containing different bifidobacterial species possessed differing amounts of oligosaccharides, suggesting differential consumption in situ.ConclusionsInfants fed by non-secretor mothers are delayed in the establishment of a bifidobacteria-laden microbiota. This delay may be due to difficulties in the infant acquiring a species of bifidobacteria able to consume the specific milk oligosaccharides delivered by the mother. This work provides mechanistic insight into how milk glycans enrich specific beneficial bacterial populations in infants and reveals clues for enhancing enrichment of bifidobacterial populations in at risk populations - such as premature infants.Electronic supplementary materialThe online version of this article (doi:10.1186/s40168-015-0071-z) contains supplementary material, which is available to authorized users.
Highlights
Individuals with inactive alleles of the fucosyltransferase 2 gene (FUT2; termed the ‘secretor’ gene) are common in many populations
This study examines the differences in infant gut microbial populations that arise from these compositional differences in human milk glycans (HMGs)
Aside from the levels of secretor status marker oligosaccharides, milk determined to be from non-secretor mothers showed other significant differences in glycan composition when compared to secretor milk over all four time points (Table 1)
Summary
Individuals with inactive alleles of the fucosyltransferase 2 gene (FUT2; termed the ‘secretor’ gene) are common in many populations. Some members of the genus Bifidobacterium, common infant gut commensals, are known to consume 2′-fucosylated glycans found in the breast milk of secretor mothers. Bifidobacteria are not alone in their ability to consume HMOs, as members of the genus Bacteroides are known to consume some types of HMOs [18]. These two groups are both involved in the production of short-chain fatty acids and lactate, which alter the pH of the environment, modulate the microbiota, and have other systemic properties [19]. Among the genes that build HMGs in the mammary gland is the fucosyltransferase 2 (FUT2) gene, which catalyzes the transfer of fucose residues by an α1,2-linkage to glycans found in human milk. The amount of fucosylation in breast milk is known to change over the course of lactation [31], which may affect the protection conferred to an infant over time
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