Abstract

Lactating mothers secrete milk sialyloligosaccharides (MSOs) that function as anti-adhesives once provided to the neonate. Particular infant-associated commensals, such as Bifidobacterium longum subsp. infantis, consume neutral milk oligosaccharides, although their ability to utilize acidic oligosaccharides has not been assessed. Temporal glycoprofiling of acidic HMO consumed during fermentation demonstrated a single composition, with several isomers, corresponding to sialylated lacto-N-tetraose. To utilize MSO, B. longum subsp. infantis deploys a sialidase that cleaves α2-6 and α2-3 linkages. NanH2, encoded within the HMO catabolic cluster is up-regulated during HMO fermentation and is active on sialylated lacto-N-tetraose. These results demonstrate that commensal microorganisms do utilize MSO, a substrate that may be enriched in the distal gastrointestinal tract.

Highlights

  • Tion of acidic human milk oligosaccharide (HMO) or milk sialyloligosaccharides (MSOs) requires cleavage of terminal ␣2– 6- and ␣2–3-linked sialyl moieties [1]

  • Our recent work detailed the composition and distribution of oligosaccharides secreted into milk [2], demonstrated that specific bifidobacteria exploit HMO as a growth substrate [2, 19], precisely identified preferred neutral oligosaccharides [15, 20] and reconstructed HMO metabolic pathways encoded by B. longum subsp. infantis ATCC15697 [21]

  • Repression of SLNT utilization by neutral milk oligosaccharides was not observed, this cannot be excluded for the other MSO compositions

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Summary

Introduction

Tion of acidic HMOs or milk sialyloligosaccharides (MSOs) requires cleavage of terminal ␣2– 6- and ␣2–3-linked sialyl moieties [1]. Human milk is a rich source of sialylated glycans, previously determined to be over 40 structures (of over 200 total HMOs) representing nearly 16% of soluble oligosaccharide abundances [2, 3]. Our recent work detailed the composition and distribution of oligosaccharides secreted into milk [2], demonstrated that specific bifidobacteria exploit HMO as a growth substrate [2, 19], precisely identified preferred neutral oligosaccharides [15, 20] and reconstructed HMO metabolic pathways encoded by B. longum subsp.

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