Nina Kirmiz, University of California, Davis, USA
Nina Kirmiz1, Daniel Garrido1, Daniele Lemay1, Santiago Ruiz-Moyano1, Jasmine Davis1, Sarah Totten1,
Jennifer Smilowitz1, J. Bruce German1, Carlito B. Lebrilla1, and David A. Mills1
1. University of California, Davis
Human milk oligosaccharides (HMO) are an abundant component of human breast milk. Bifidobacterium is often reported as a predominant genus in the microbiota of breast-fed infants and it is believed that bifidobacteria provide positive health benefits. Previous work has shown that strains of Bifidobacterium longum subsp. infantis (B. infantis) and Bifidobacterium bifidum have the ability to grow to high cell densities on HMO as a sole carbon source and the molecular mechanisms of HMO consumption by B. infantis and B. bifidum have been previously described. Until recently, HMO consumption by Bifidobacterium longum subsp. longum and Bifidobacterium breve has been described to a lesser extent. We have isolated two strains, B. longum subsp. longum SC596 and B. breve SC95, which can grow well on pooled HMO and individual HMO sugars as a sole carbon source. Genome analysis, transcriptomics, and functional studies were used to examine HMO consumption by B. longum subsp. longum SC596 and B. breve SC95. B. longum subsp. longum SC596 and B. breve SC95 possess a range of glycosyl hydrolases and oligosaccharide transporters induced during growth on HMO. Various glycosyl hydrolases purified from these strains have activity on HMO linkages and the family 1 solute binding proteins bind to HMO. Furthermore, we characterize a gene cluster B. longum subsp. longum SC596 possesses that allows for utilization of fucosylated HMO. This work provides insight into classes of B. longum subsp. longum and B. breve that are HMO responders. This work provides a mechanism for how select strains of bifidobacteria vigorously consume HMO, which may enhance their ability to colonize breastfed infants.