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Microbiome. 2015 Apr 10;3:13. doi: 10.1186/s40168-015-0071-z. eCollection 2015.

Maternal fucosyltransferase 2 status affects the gut bifidobacterial communities of breastfed infants.

Author information

1
Department of Food Science and Technology, UC Davis, 1 Shields Avenue, Davis, CA 95616 USA ; Foods For Health Institute, UC Davis, 1 Peter J Shields Avenue, Davis, CA 95616 USA.
2
Department of Chemistry, UC Davis, 1 Shields Avenue, Davis, CA 95616 USA ; Foods For Health Institute, UC Davis, 1 Peter J Shields Avenue, Davis, CA 95616 USA.
3
Department of Life Sciences, PhD School in Science and Technologies for Health Products, University of Modena and Reggio Emilia, Via Università, 4, Modena, MO 41100 Italy.
4
Department of Chemistry, UC Davis, 1 Shields Avenue, Davis, CA 95616 USA.
5
Genome Center, UC Davis, 1 Shields Avenue, Davis, CA 95616 USA.
6
Department of Food Science and Human Nutrition, University Illinois at Urbana-Champaign, S. Goodwin Ave., Urbana, IL 61801 USA.
7
Department of Food Science and Technology, UC Davis, 1 Shields Avenue, Davis, CA 95616 USA ; Department of Viticulture and Enology, UC Davis, 1 Shields Avenue, Davis, CA 95616 USA ; Foods For Health Institute, UC Davis, 1 Peter J Shields Avenue, Davis, CA 95616 USA.

Abstract

BACKGROUND:

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. We investigated the effects of maternal secretor status on the developing infant microbiota with a special emphasis on bifidobacterial species abundance.

RESULTS:

On 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.

CONCLUSIONS:

Infants 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.

KEYWORDS:

Bifidobacteria; Breastfeeding; FUT2; Human milk oligosaccharides; Infant; Marker gene sequencing; Secretor; Short-chain fatty acids

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