Abstract
Much evidence suggests a role for human milk oligosaccharides (HMOs) in establishing the infant microbiota in the large intestine, but the response of particular bacteria to individual HMOs is not well known. Here twelve bacterial strains belonging to the genera Bifidobacterium, Enterococcus, Limosilactobacillus, Lactobacillus, Lacticaseibacillus, Staphylococcus and Streptococcus were isolated from infant faeces and their growth was analyzed in the presence of the major HMOs, 2′-fucosyllactose (2′FL), 3-fucosyllactose (3FL), 2′,3-difucosyllactose (DFL), lacto-N-tetraose (LNT) and lacto-N-neo-tetraose (LNnT), present in human milk. Only the isolated Bifidobacterium strains demonstrated the capability to utilize these HMOs as carbon sources. Bifidobacterium infantis Y538 efficiently consumed all tested HMOs. Contrarily, Bifidobacterium dentium strains Y510 and Y521 just metabolized LNT and LNnT. Both tetra-saccharides are hydrolyzed into galactose and lacto-N-triose (LNTII) by B. dentium. Interestingly, this species consumed only the galactose moiety during growth on LNT or LNnT, and excreted the LNTII moiety. Two β-galactosidases were characterized from B. dentium Y510, Bdg42A showed the highest activity towards LNT, hydrolyzing it into galactose and LNTII, and Bdg2A towards lactose, degrading efficiently also 6′-galactopyranosyl-N-acetylglucosamine, N-acetyl-lactosamine and LNnT. The work presented here supports the hypothesis that HMOs are mainly metabolized by Bifidobacterium species in the infant gut.
Highlights
Human milk oligosaccharides (HMOs) are non-conjugated and structurally diverse carbohydrates present in human milk, with more than 100 structures already e lucidated[1]
Based on partial 16S rRNA gene sequencing, the isolates were identified as Bifidobacterium dentium (Y510, Y521, Y522, Y525, Y546), Bifidobacterium longum (Y538), Enterococcus faecalis (Y513, Y515-516, Y530-534, Y536, Y547-548, Y550), Limosilactobacillus fermentum (Y500, Y502, Y504, Y506-509, Y512, Y523-524, Y527-528, Y535, Y537), Lactobacillus gasseri (Y511), Lacticaseibacillus paracasei (Y526), Limosilactobacillus reuteri (Y501, Y503, Y505), Staphylococcus epidermidis (Y520), Staphylococcus hominis (Y549) and Streptococcus pasteurianus (Y529)
human milk oligosaccharides (HMOs) have been proposed as the main metabolites from human milk that directly influence the microbiota composition of the infant gastrointestinal t ract[9,10]
Summary
Human milk oligosaccharides (HMOs) are non-conjugated and structurally diverse carbohydrates present in human milk, with more than 100 structures already e lucidated[1] They constitute the third solid component most abundant in human milk after lactose and lipids. Infantis, Bifidobacterium bifidum and Bifidobacterium breve readily utilize HMOs10,12–15. They have been shown to possess a great battery of glycosyl hydrolases involved in the catabolism of specific H MOs10,15–18. Bacteria were isolated from breastfed infant faeces and their capability to utilize major individual HMOs (2′FL, 3FL, DFL, LNT and LNnT), HMO-derived glycans and monosaccharides for growth was determined. The Bifidobacterium infantis strain Y538 was found to be the most efficient at consuming all tested HMOs, and the Bifidobacterium dentium strains Y510 and Y521 were able to ferment the galactose moiety of LNT and LNnT. Two β-galactosidases with activity in these tetrasaccharides were characterized from B. dentium
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