Journal
PEDIATRIC RESEARCH
Volume 72, Issue 1, Pages 10-18Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/pr.2012.48
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Funding
- Princess Margaret Hospital
- Women's and Infants' Research Foundation (WA)
- Clive and Vera Ramaciotti Medical Research Foundation
- University of Western Australia
- Rebecca Cooper Medical Research Foundation
- Channel 7 Telethon
- European Society for Paediatric Infectious Diseases
- National Health and Medical Research Council, Australia [513847]
- Deutsche Forschungsgemeinschaft [STR1022/1-1]
- international postgraduate research scholarship of the University of Western Australia
- BrightSpark Foundation WA Fellowship
- National Health and Medical Research Council Career Development Award
- National Institutes of Health [RO1 AI067353-01A1, R01AI067353-05S1]
- Global Health grant from The Bill & Melinda Gates Foundation [OPPGH5284]
- Harvard-Australia Fellowship
- Victorian Government's Operational Infrastructure Support Program
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INTRODUCTION: Staphylococcus epidermidis (SE) rarely causes infection in term infants but is a leading cause of late-onset sepsis in preterm infants. We hypothesized that the innate immune responses to SE in preterm infants are impaired in a gestational age (GA)-dependent manner. METHODS: Cord and peripheral blood mononuclear cells (MNCs) were stimulated with SE bacteria, and a range of innate immune responses were assessed, including phagocytosis, intracellular killing, Toll-like receptor (TLR) pathway transcriptional activation, cytokine production, TLR2 and TLR4 expression, and cell signaling. RESULTS: Phagocytosis and intracellular killing of SE bacteria were similar in neonatal and adult monocytes. Cytokine gene expression and protein synthesis increased in a GA-dependent manner, which was confirmed at the single-cell level. These GA-related effects were not associated with differences in expression of TLR2 or TLR4, nor with downstream activation of nuclear factor-kappa B or mitogen-activated protein kinase pathways. DISCUSSION: The expression of TLRs, phagocytic capacity, and intracellular killing by monocytes develops early in fetal development, whereas the ability to mount a bacteria-induced cytokine response requires further maturation. The functional immaturity of monocyte activation pathways in the preterm infant may underpin their particular susceptibility to sepsis with commensal bacteria.
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