Journal
ACS INFECTIOUS DISEASES
Volume 3, Issue 8, Pages 595-605Publisher
AMER CHEMICAL SOC
DOI: 10.1021/acsinfecdis.7b00064
Keywords
Group B Streptococcus; GBS; antimicrobial; antibiofilm; bacteriostatic; human milk oligosaccharides; HMO
Categories
Funding
- Vanderbilt University
- Department of Pediatrics at Vanderbilt University Medical Center
- Institute of Chemical Biology
- Department of Veterans Affairs [CDA-2 11K2BX001701]
- Amgen Foundation
- Mitchum E. Warren, Jr. Graduate Research Fellowship
- NIH [T32AI007474-20, 2T32HD060554-06A2]
- Vanderbilt University Core Services by Vanderbilt Institute for Clinical and Translational Research program by National Center for Research Resources [UL1 RR024975-01]
- National Center for Advancing Translational Sciences [2 UL1 TR000445-06]
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Streptococcus agalactiae (Group B Streptococcus, GBS) is a Gram-positive bacterial pathogen that causes invasive infections in both children and adults. During pregnancy, GBS is a significant cause of infection of the fetal membranes (chorioamnionitis), which can lead to intra-amniotic infection, preterm birth, stillbirth, and neonatal sepsis. Recently, breastfeeding has been thought to represent a potential mode of GBS transmission from mother to newborn, which might increase the risk for late-onset sepsis. Little is known, however, about the molecular components of breast milk that may support or prevent GBS colonization. In this study, we examine how human milk oligosaccharides (HMOs) affect the pathogenesis of GBS. HMOs from discrete donor samples were isolated and profiled by matrix-assisted laser desorption/ionization (MALDI) mass spectrometry (MS). Growth and biofilm assays show that HMOs from mothers of specific milk groups can modulate the growth and biofilm formation of GBS. High-resolution field-emission gun scanning electron microscopy (SEM) and confocal laser scanning microscopy confirmed the quantitative biofilm assays and demonstrated cell arrangement perturbations in bacterial cultures treated with specific oligosaccharides. These findings demonstrate that HMOs affect the growth and cell biology of GBS. Finally, this study provides the first example of HMOs functioning as antibiofilm agents against GBS.
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