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Published (Version of Record)CC BY V4.0, Open Access
Journal article
Characterising commensal and pathogenic staphylococcal interactions with neonatal and adult blood
Scientific reports, Vol.16(1), 777
2026
PMID: 41366267
Abstract
The abundant skin commensal, Staphylococcus epidermidis, is the leading cause of late-onset sepsis (LOS) in preterm infants but rarely causes infections in term infants and adults. Staphylococcal virulence mechanisms and the role of the preterm immune responses in driving these life-threatening infections remain poorly understood. Using an ex vivo sepsis model, we challenged whole blood from very preterm infants (30-32 weeks gestational age, GA; n = 8), term infants (> 37 weeks GA; n = 8), and young adults (18-25 years; n = 8) with either live S. epidermidis or S. aureus (~ 10
colony-forming units, CFU/ml) for 90 min. Dual RNA-sequencing (RNA-seq) was performed to simultaneously assess host and pathogen gene expression profiles, identifying common and pathogen-specific responses across cohorts. We found shared immune processes induced in all age groups upon bacterial challenge, including cytokine (IL1A, IL1B, IL6, IFNB1) and chemokine (CCL20, CCL3, CCL7, CXCL2) signalling. Preterm infants also exhibited unique responses, such as increased platelet activation and fibrin clot formation, Wnt signalling, and hypoxia pathways in response to S. epidermidis challenge. Our findings suggest that bacterial gene co-expression, including iron acquisition and heme biosynthesis genes, are also influenced by the hosts developmental age, highlighting the complexity of host-bacterial interactions in the early stages of neonatal sepsis.
Details
- Title
- Characterising commensal and pathogenic staphylococcal interactions with neonatal and adult blood
- Authors/Creators
- Isabella Anna Joubert - Murdoch UniversityChristopher Mullally - Murdoch UniversityPenghao Wang - Murdoch UniversityAbha Chopra - Murdoch UniversityTobias Strunk - Mécanique et Engrenage ModerneAndrew Currie - Murdoch University
- Publication Details
- Scientific reports, Vol.16(1), 777
- Publisher
- Springer Nature; BERLIN
- Number of pages
- 15
- Identifiers
- 991005838666907891
- Copyright
- © The Author(s) 2025
- Murdoch Affiliation
- School of Medical, Molecular and Forensic Sciences; Personalised Medicine Centre
- Language
- English
- Resource Type
- Journal article
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