oligosaccharides (LoCascio et al., 2007; Ward et al., 2007). Only an estimated 4 to 38 percent of HMOs are sialyated; a higher proportion are fucosylated (40 to 70 percent) (Ninonuevo et al., 2006). Moreover, Mills’s team has also identified which B. infantis genes cleave what HMO linkages (Sela et al., 2011). Interestingly, in German’s opinion, the expression of the bacterial enzyme that actually cleaves the sialyated oligosaccharides is regulated by the abundance of HMOs in the growth medium. There is other evidence indicating that human milk sugars interact with the microbiome in ways that increase the value of the microbiome to the infant. For example, German mentioned the research of Helen Raybould’s group on B. infantis and its role in endocrine signaling in the infant intestine (Chichlowski et al., 2012).

The real question, in German’s opinion, is whether the association between HMOs and B. infantis persists as a phenotype in “real life.” That is, “does is really influence the bacteria in living babies?” Data on microbiome development through the first 12 weeks of an infant’s life show that initially Bifidobacterium is not present in the microbiome (manuscript in preparation), but by week 12 it emerges as a dominant member of the microbiome. Evidence from fecal sampling indicates that HMOs are not being digested during the first weeks of life, presumably because there are no bifidobacteria to digest them, but they begin to disappear from the infant feces at the same time Bifidobacterium begins to dominate the microbiome (manuscript in preparation). Thus, the association between HMOs and B. infantis is a “true symbiotic relationship,” German said. “It’s as important to feed the bacteria in the baby as the baby.”

German suggested that knowledge of human milk–microbiome symbiosis could be translated into practice in several ways. For example, he mentioned Mark Underwood’s research on the effects of administering a combination of B. infantis and HMOs to premature infants (manuscript in preparation).


There are very few data on the development of the gut microbiota in healthy infants, let alone how diet impacts that microbiota. Yet, there is a plethora of clinical and epidemiological data suggesting that breast-feeding promotes mucosal immune development and protects against many diseases. These data, combined with the fact that human milk contains a variety of bioactive proteins, carbohydrates, and lipids not present in infant formula, raise questions about whether and how the infant gut microbiota differs between breast-fed and formula-fed infants. Sharon Donovan’s long-term


3 This section summarizes the presentation of Sharon Donovan.

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