Metabolization of human milk oligosaccharides by Streptococcus pneumoniae
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Updated: Oct 31, 2026

Analysis of Fucosylated Human Milk Trisaccharides in Biotechnological Context Using Genetically Encoded Biosensors
Published on: April 13, 2019
Katharina Bacher1,2, Ustina Martysiuk1,2, Greicy K Bonifacio-Pereira3
1Institute for Infectious Diseases, Faculty of Medicine, University of Bern, Bern, Switzerland.
Abstract:
It is unclear whether human milk oligosaccharides (HMOs) can be used as a nutrient source by Streptococcus pneumoniae. Here, we investigate whether and how S. pneumoniae metabolizes HMOs and whether these compounds inhibit pneumococcal adherence. We find that S. pneumoniae can metabolize several HMOs, except for 2'-fucosyllactose (2'FL). The process is regulated by the carbon catabolite repression system. Transcriptome analyses showed reduced expression of the lac operon I (lacABCD) in bacteria grown with two tested HMOs when compared to lactose (Lac). Genes for the Leloir pathway and exoglycosidases were upregulated. A genome-wide CRISPR interference screen showed that the lac operons I and II (lacEFG-2) are essential for metabolizing HMOs. Lac and non-metabolizable 2'FL were found to inhibit pneumococcal adherence to host cells in vitro. Importantly, 2'FL showed a stronger inhibitory effect compared to Lac in vivo. Further research is warranted to investigate whether the non-metabolizable 2'FL can be used to inhibit pneumococcal adherence.
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