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Updated: Feb 18, 2026
Isolation and Characterization of Human Umbilical Cord-derived Mesenchymal Stem Cells from Preterm and Term Infants
Published on: January 26, 2019
Identification of generic and pathogen-specific cord blood monocyte transcriptomes reveals a largely conserved
Emma de Jong1, David G Hancock2, Julie Hibbert3
1Medical & Molecular Sciences, School of Veterinary & Life Sciences, Murdoch University, South Street, Murdoch, Western Australia, 6150, Australia. emma.dejong@outlook.com.
Insights
Neonatal monocytes mount a conserved transcriptional response to E. coli and S. epidermidis, primarily via TLR/NF-κB/TREM-1 signaling. Interferon genes are differentially regulated, with responses largely unaffected by gestational age or chorioamnionitis.
Area of Science:
- Immunology
- Neonatal Medicine
- Genomics
Background:
- Neonatal sepsis, often caused by E. coli and S. epidermidis, disproportionately affects preterm infants.
- Immature innate monocyte defenses are implicated, but their global transcriptional responses to these pathogens are uncharacterized.
- Understanding these responses is crucial for developing targeted interventions against neonatal sepsis.
Purpose of the Study:
- To identify and characterize neonatal monocyte transcriptional responses to E. coli and S. epidermidis.
- To investigate the influence of gestational age and chorioamnionitis exposure on these responses.
- To elucidate the signaling pathways involved in neonatal monocyte defense mechanisms.
Main Methods:
- Purified cord blood monocytes from very preterm (<32 weeks GA) and term (37-40 weeks GA) infants were used.
- Monocytes were challenged with live S. epidermidis or E. coli.
- Global transcriptional responses were assessed using RNA-sequencing.
Main Results:
- Both pathogens induced highly conserved transcriptional changes in neonatal monocytes, indicating a common response pathway.
- The primary signaling pathways involved were Toll-like receptor (TLR)/NF-κB/TREM-1.
- E. coli specifically triggered an interferon-centered immune response in both preterm and term infant monocytes, distinct from S. epidermidis.
Conclusions:
- Neonatal monocytes exhibit a conserved transcriptional response to common sepsis pathogens, mediated by TLR/NF-κB/TREM-1 signaling.
- Differential regulation of interferon genes by E. coli and S. epidermidis was observed.
- These immune responses were largely independent of gestational age and prior chorioamnionitis exposure.
Abstract:
Escherichia coli and Staphylococcus epidermidis are predominant causes of neonatal sepsis, particularly affecting preterm infants. Susceptibility to infection has been attributed to "immature" innate monocyte defences, but no studies have assessed global transcriptional responses of neonatal monocytes to these pathogens. Here, we aimed to identify and characterise the neonatal monocyte transcriptional responses to E. coli and S. epidermidis and the role of common modifiers such as gestational age (GA) and exposure to chorioamnionitis (a common complication of preterm birth) to better understand early life innate immune responses. RNA-sequencing was performed on purified cord blood monocytes from very preterm (< 32 weeks GA) and term infants (37-40 weeks GA) following standardised challenge with live S. epidermidis or E. coli. The major transcriptional changes induced by either pathogen were highly conserved between infant groups and stimuli, highlighting a common extant neonatal monocyte response to infection, largely mediated by TLR/NF-κB/TREM-1 signalling. In addition, we observed an activated interferon-centred immune response specific to stimulation with E. coli in both preterm and term infants. These data provide novel insights into the functionality of neonatal monocytes at birth and highlight potential pathways that could be targeted to reduce the harmful effects of bacterial-induced inflammation in sepsis. E. coli and S. epidermidis elicit common transcriptional changes in cord monocytes. The common transcriptional response is mediated by TLR/NF-κB/TREM-1 signalling. IFN genes are differentially regulated by E. coli and S. epidermidis in monocytes. These responses are largely unaffected by GA or exposure to chorioamnionitis.
Key Messages:
E. coli and S. epidermidis elicit common transcriptional changes in cord monocytes. The common transcriptional response is mediated by TLR/NF-κB/TREM-1 signalling. IFN-genes are differentially regulated by E. coli and S. epidermidis in monocytes. These responses are largely unaffected by GA or exposure to chorioamnionitis.
