Human milk oligosaccharides inhibit growth of group B Streptococcus [Glycobiology and Extracellular Matrices]

Streptococcus agalactiae (group B Streptococcus; GBS) is a leading cause of invasive bacterial infections in newborns, typically acquired vertically during childbirth secondary to maternal vaginal colonization. Human milk oligosaccharides (HMOs) have important nutritional and biological activities that guide development of the infant's immune system and shape the composition of normal gut microbiota. In this manner, HMOs help protect against pathogen colonization and reduce risk of infection. In the course of our studies of HMO-microbial interactions, we unexpectedly uncovered a novel HMO property to directly inhibit the growth of GBS, independent of host immunity. By separating different HMO fractions through multi-dimensional chromatography, we found the bacteriostatic activity to be confined to specific non-sialylated HMOs, and synergistic with a number of conventional antibiotic agents. Phenotypic screening of a GBS transposon insertion library identified a mutation within a GBS-specific gene encoding a putative glycosyltransferase that confers resistance to HMOs, suggesting HMOs may function as alternative substrate to modify a GBS component in a manner that impairs growth kinetics. Our study uncovers a unique antibacterial role for HMOs against a leading neonatal pathogen, and expands the potential therapeutic utility of these versatile molecules.

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