Adaptive response of neonatal sepsis-derived Group B Streptococcus to bilirubin

Richard Hansen* (Corresponding Author), Sophie Gibson, Eduardo De Paiva Alves, Mark Goddard, Andrew MacLaren, Anne Marie Karcher, Susan Berry, Elaina S. R. Collie-Duguid, Emad El-Omar, Mike Munro, Georgina L. Hold

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

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Hyperbilirubinemia is so common in newborns as to be termed physiological. The most common bacteria involved in early-onset neonatal sepsis are Streptococcus agalactiae, commonly called Group B Streptococcus (GBS). Whilst previous studies show bilirubin has antioxidant properties and is beneficial in endotoxic shock, little thought has been given to whether bilirubin might have antibacterial properties. In this study, we performed a transcriptomic and proteomic assessment of GBS cultured in the presence/absence of bilirubin. Our analysis revealed that increasing levels of bilirubin (>100 µmol/L) negatively correlated with GBS growth (18% reduction from 0–400 µmol/L on plate model, p < 0.001; 33% reduction from 0–100 µmol/L in liquid model, p = 0.02). Transcriptome analysis demonstrated 19 differentially expressed genes, almost exclusively up-regulated in the presence of bilirubin. Proteomic analysis identified 12 differentially expressed proteins, half over-expressed in the presence of bilirubin. Functional analysis using Gene Ontology and KEGG pathways18 revealed a differential expression of genes involved in transport and carbohydrate metabolism, suggesting bilirubin may impact on substrate utilisation. The data improve our understanding of the mechanisms modulating GBS survival in neonatal hyperbilirubinemia and suggest physiological jaundice may have an evolutionary role in protection against early-onset neonatal sepsis.
Original languageEnglish
Article number6470
Pages (from-to)1-10
Number of pages10
JournalScientific Reports
Publication statusPublished - 24 Apr 2018

Bibliographical note

This work was funded by the Neonatal Unit Endowment Fund, Aberdeen Maternity Hospital. RH is funded by a career researcher fellowship from NHS Research Scotland. SG was funded by the MRC Flagship PhD programme. We are grateful for the support of Dr Phil Cash and Aberdeen Proteomics, at University of Aberdeen,
in completing this project.
Supplementary information accompanies this paper at


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