Studies have shown that viruses, bacteria, and protozoan pathogens must first adhere to the mucosal surface before they can colonize and invade the host, leading to disease[1].

HMOs (Human Milk Oligosaccharides) share similar antigenic determinants with the sugar chain structures on the surface of intestinal mucosal cells. These act as analogs of lectin ligands, preventing pathogens from binding to intestinal epithelial cells. This reduces the risk of viral and bacterial infections and lowers the incidence of infectious diseases[2].

HMOs (Human Milk Oligosaccharides) are a group of carbohydrates that are resistant to digestive breakdown in the gut. When infants orally consume HMOs, approximately 99% of them reach the colon and distal small intestine intact and in high concentrations. Of these, 45% are fermented by the gut microbiota, while 1%-4% are excreted in urine, and 40%-50% are excreted in feces[2].

HMOs act as soluble receptor traps for viruses. Once pathogens adhere to these receptors, HMOs can trap and carry them out of the body through processes like adhesion and encapsulation, thereby reducing the risk of subsequent infections.

The health of the intestinal tract and its barrier function represent the first line of defense in a baby’s innate immunity.

Daily factors such as diet, bacteria, viruses, medications, environmental pollutants, and emotional stress can influence the intestinal microbial environment and mucosal barrier. These changes may lead to microbial dysbiosis or damage to the mucus layer, increasing the risk of subsequent diseases[2-4].

HMOs (Human Milk Oligosaccharides) structurally resemble mucin glycans and can serve as substrates for mucinophilic bacteria, thereby reducing excessive mucin depletion. Studies have shown that short-chain fatty acids (SCFAs), the metabolic byproducts of HMOs, promote intestinal epithelial cell maturation and stimulate mucin secretion. This helps mitigate mucus layer thinning and microbial translocation, thereby supporting the regulation of the intestinal mucosal barrier[5].

Beyond the mucus barrier, the intestinal mechanical and immune barriers also play vital roles. Research has shown that HMOs (Human Milk Oligosaccharides) support intestinal integrity by enhancing tight junctions.

The short-chain fatty acids (SCFAs) produced from HMO metabolism can alter the glycosylation patterns on epithelial cell surfaces, reducing pathogen adhesion and promoting colonic epithelial repair and innate immune homeostasis. Additionally, HMOs increase the expression of antimicrobial peptides in colonic epithelial cells, regulate T-cell numbers and activity, and suppress the aggregation and pro-inflammatory activity of neutrophils, macrophages, dendritic cells, and effector T-cells. These effects collectively modulate the intestinal immune and mechanical barrier functions[2].

Studies show that short-chain fatty acids (SCFAs), which are metabolic by-products of HMOs, serve as an energy source for colon cells and certain microbiota. They lower the luminal pH, helping to create an acidic environment in the gut, which in turn inhibits the growth of pathogens in the intestines[2].

In breastfed infants, Bifidobacteria dominate the gut microbiota, accounting for 80-90% of the microbial composition. However, this abundance decreases rapidly after breastfeeding stops[3]. Research has confirmed that Bacteroides and Bifidobacteria efficiently use HMOs as a carbon source, increasing their abundance[4].

More importantly, HMOs selectively support the growth of beneficial bacteria that are beneficial to the infant's health, while not being utilized by harmful pathogens[3-5].