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Updated: Jun 4, 2026

A Neonatal Imaging Model of Gram-Negative Bacterial Sepsis
Published on: August 12, 2020
The effect of hyperglycemia on neonatal immune responses in-vitro
Petra Temming1, Birte Tröger, Susanne Thonnissen
1Department of Paediatrics, University Hospital Schleswig-Holstein, Campus Lübeck, Germany.
Insights
Acute hyperglycemia may increase pro-inflammatory cytokines like IL-8 in neonatal blood. This suggests glucose control is vital for infant health, impacting inflammatory responses.
Area of Science:
- Neonatal immunology
- Endocrinology
- Critical care medicine
Background:
- Acute hyperglycemia is a pro-inflammatory state linked to poor outcomes in critically ill adults.
- Neonates are vulnerable to infections and inflammatory responses.
- This study investigates the link between neonatal glucose regulation and inflammatory cytokine production.
Purpose of the Study:
- To examine the in-vitro effects of hyperglycemia and insulin on pro-inflammatory cytokine production in neonatal and adult blood.
- To understand the role of glucose homeostasis in neonatal inflammatory responses.
Main Methods:
- Whole cord blood from term infants, preterm infants (<32 weeks and >32 weeks gestational age), and adult controls was used.
- Blood samples were incubated with varying glucose and insulin concentrations and stimulated with lipopolysaccharide.
- Intracytoplasmic tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-8 (IL-8) were measured via flow cytometry.
Main Results:
- In-vitro hyperglycemia dose-dependently increased IL-8 in all groups.
- Glucose stimulated TNF-α in preterm infants (≤32 weeks) and term infants.
- Insulin had no significant effect on pro-inflammatory cytokine production.
Conclusions:
- Acute hyperglycemia can induce pro-inflammatory cytokine responses in neonatal blood.
- Findings support further research into glucose homeostasis's impact on neonatal outcomes.
- Data provides a foundation for in-vitro and in-vivo studies on neonatal inflammatory responses.
Introduction:
Acute hyperglycemia is considered as a pro-inflammatory state and is related to an adverse outcome in critically ill adults. Neonates are susceptible to infections and systemic inflammatory response syndrome induced by pro-inflammatory cytokines. This study focuses on the interaction between neonatal glucose homeostasis and the pro-inflammatory cytokine production in term and preterm infants in-vitro.
Methods:
We analyzed the pro-inflammatory cytokine production in whole cord blood of term infants (n = 10), preterm infants > 32 weeks (n=16) and preterm infants ≤32 weeks of gestational age (n = 13) and in adult controls (n=14) using an in-vitro sepsis-model. Whole blood was pre-incubated with different concentrations of glucose (0-1000 mg/dl) and insulin (0-62.5 IE/l) and stimulated with lipopolysaccharide. The intracytoplasmatic TNF-α, IL-6, and IL-8 response was measured by flow cytometry.
Results:
In-vitro hyperglycemia induced a dose-dependent increase of IL-8 in all age groups while TNF-α was demonstrated to be stimulated by glucose in cord blood samples of preterm infants ≤32 weeks of gestational age and term infants. In contrast, insulin showed no significant effects on pro-inflammatory cytokine production in-vitro.
Conclusion:
Acute hyperglycemia may induce pro-inflammatory cytokine responses in neonatal whole blood in-vitro. These data provide a basis for further in-vitro signal transduction studies and in-vivo investigations about the significance of neonatal glucose homeostasis and its impact on long-term outcome of this susceptible patient cohort.
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