Human milk oligosaccharides (HMOs) are complex glycans and the third-largest solid component in human milk. They are typically nondigestible by humans but are a major substrate for infants’ gut microbiota and affect the maturation of the intestinal mucosal immune system.
All HMOs are extensions of lactose generated by the action of a series of glycosyltransferases. Depending on the mother’s Secretor and Lewis blood groups, the fucosyltransferases FUT2 (the Secretor gene) and/or FUT3 (the Lewis gene) are available for the synthesis of HMOs. The resulting heterogeneity implies that some breastfed infants are not being exposed to certain structures, which may affect their microbiome composition and thereby disease risk for illnesses in which gut microbiome plays a role.
Infants fed by mothers who lack a Secretor gene and therefore lack a functional FUT2 enzyme and all α-1-2-fucosylated oligosaccharides have delayed development of bifidobacteria-laden microbiota. Also, if these infants are born via cesarean delivery, they have a higher risk to manifest IgE-associated eczema.
We recently showed that certain HMOs are associated with protection against cow-milk allergy in infants. Besides genetic differences that are responsible for differences in HMO profiles, HMO abundance changes throughout lactation. However, no other factors have been associated with variation in HMO abundances.
This study sought to assess the association of maternal probiotic supplementation with HMO concentrations.
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