Human milk oligosaccharides: Every baby needs a sugar mama
Abstract
Human milk oligosaccharides (HMOs) are a family of structurally diverse unconjugated glycans that are highly abundant in and unique to human milk. Originally, HMOs were discovered as a prebiotic “bifidus factor” that serves as a metabolic substrate for desired bacteria and shapes an intestinal microbiota composition with health benefits for the breast-fed neonate. Today, HMOs are known to be more than just “food for bugs”. An accumulating body of evidence suggests that HMOs are antiadhesive antimicrobials that serve as soluble decoy receptors, prevent pathogen attachment to infant mucosal surfaces and lower the risk for viral, bacterial and protozoan parasite infections. In addition, HMOs may modulate epithelial and immune cell responses, reduce excessive mucosal leukocyte infiltration and activation, lower the risk for necrotizing enterocolitis and provide the infant with sialic acid as a potentially essential nutrient for brain development and cognition. Most data, however, stem from in vitro, ex vivo or animal studies and occasionally from association studies in mother–infant cohorts. Powered, randomized and controlled intervention studies will be needed to confirm relevance for human neonates. The first part of this review introduces the pioneers in HMO research, outlines HMO structural diversity and describes what is known about HMO biosynthesis in the mother's mammary gland and their metabolism in the breast-fed infant. The second part highlights the postulated beneficial effects of HMO for the breast-fed neonate, compares HMOs with oligosaccharides in the milk of other mammals and in infant formula and summarizes the current roadblocks and future opportunities for HMO research.
Data from Hale and Hartmann (2007).
Data complied from the following references: Coppa et al. (1999), Kunz et al. (1999), Newburg et al. (2000), Chaturvedi, Warren, Altaye, et al. (2001), Davidson et al. (2004), Bao et al. (2007) and Gabrielli et al. (2011).
Data from Gopal and Gill (2000).
Data complied from the following references Ninonuevo et al. (2006) and Wu et al. (2010; 2011) and reviewed in Kobata (2010).
Data from Tao et al. (2008) and Tao et al. (2009).
Depending on the woman's Se/Le blood group status.
Acknowledgements
I expresses my deepest gratitude to my PhD advisors Clemens Kunz and Silvia Rudloff at the Justus-Liebig-University in Giessen, Germany, who initiated my excitement for HMO research, to my postdoctoral advisor Hudson Freeze at the Burnham Institute in La Jolla, CA, who taught me the essentials of glycobiology and to Ajit Varki and Jeff Esko at the University of California, San Diego, for their continuous inspiration and support. I thank the dedicated and hard working members of my lab at the University of California, San Diego, better known as the “Milk Gang”.