人乳寡糖系列 ---乳糖-N-四糖 相关产品参考，更多请电话/ 微信 13296136554
Human Milk Oligosaccharides
Our Human Milk Oligosaccharides includes the range shown in Table 1
Human breast milk provides the primary source of nutrition for
newborns before they are able to eat and digest other foods. One
distinctive property of human milk from most other species is the amount
and diversity of the free oligosaccharide it contains. These human milk
oligosaccharides (HMO) can be present at levels of up to 12 g/l in milk
and up to 20 g/l in colostrum.1 HMO have been attributed with a variety of functions including:
1) Prebiotic
2) Decoy carbohydrate
3) Immunomodulation
人乳寡糖系列 ---乳糖-N-四糖 相关产品参考，更多请电话/ 微信 13296136554
HMO Structure
Currently at least 130 unique HMO have been identified, all differing
by constituent sugars, molecular weight or structure. Many share a
common motif characterized by repetitive attachment of galactose (Gal)
and N-acetylglucosamine (GlcNAc)2 in a b-glycosidic linkage
to lactose. Additional variety is generated by the addition of fucose
(termed neutral HMO), e.g. 3'-Fucosyllactose, (05673) or
2-Fucosyllactose, (06739) and sialic acid (termed acidic HMO), e.g.
6'-Sialyllactose, (04398) and 3'-Sialyllactose, (04397). Addition is via
a-glucosidic bonds to generate oligosaccharides from three to thirty
two sugars in length. Whilst most of the biosyntheis of HMO is not
controlled at the gene level (unlike proteins) the presence and position
of fucosylation is governed by the Lewis/Secretor status of the mother.3
Dominant neutral oligosaccharides have been identified as
lacto-N-tetraose (05683), lacto-N-neotetraose (05765) and
lacto-N-fucopentaose I and V (05676 and 06817 respectively)4
Prebiotic Properties of HMO
The most abundant HMO is lacto-N-tetraose which is able to survive
the acid environment of the stomach and is not degraded by normal gut
enzymes. It therefore can pass down to the lower intestine where it acts
as a prebiotic which encourages lower gut colonisation by many
bifidobacteria species, which are recognised as essential for normal gut
function.5
HMO as Decoy Carbohydrates
Binding to a host cell wall is critical for the virulence of many pathogenic bacteria including Campylobacter jejuni, E.coli, Vibrio cholera, and Shigella and some Salmonella strains. Many of the virulence factors of these organisms are
carbohydrate-binding proteins (lectins) which bind sugars displayed on
cell membranes. HMO can bind to these lectins acting as decoys and
preventing pathogens from sticking to the target cells. An example of
this is the inverse relationship between the incidence of C. jejuni,
(one of the most predominant causes of diarrhoea in the world) in
breast-fed children and levels of 2-fucosyl-lactose in the mother’s
milk. (C. jejuni is known to adhere to intestinal 2-fucosyl-lactosamine).6 Similar antimicrobial effects of HMO have also been demonstrated for
calicivirus diarrhoea and infections with heat stable enterotoxin of E. coli.7
During ingestion, HMO coat the throat and are known to inhibit adhesion of Streptococcus pneumoniae and Haemophilus influenzae to human pharyngeal or buccal epithelial cells resulting in the lower
incidence of otitis media (inner ear infection) in breast fed babies.8
Immune Role of HMO
Selectins are glycoproteins which are displayed on the surface of
many cells of the immune system and are involved with cell/cell
interactions such as the infiltration of tissues in inflammation.
Selectins bind to specific fucosylated and sialylated oligosaccharides,
e.g., sialyl Lewis x (sLex, 04058), on their respective
target ligands. HMO share many structural similarities to these
carbohydrate ligands and acidic (sialylated) HMO are able to inhibit
rolling and adhesion of leucocytes at physiologically relevant
concentrations.
One of these selectin interactions is the formation of
platelet/neutrophil complexes (PNCs) which lead to the activation of the
neutrophils. PNCs are thought to be involved in necrotizing
enterocolitis (NEC) and HMO have been attributed as the agent
responsible for the lower incidence of NEC in breast fed infants (85 %
lower than formula fed infants) via inhibition of PNC formation.9
Fractions of HMO are also known to inhibit the binding of both
Galectins which bind b-Gal and LAcNAc terminated glycans and Siglecs
which are specific for terminal sialic acid, their role in immunity or
development however has not yet been fully explored.10,1
