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Harnessing the glycolysis-TCA cycle axis to boost host defense against neonatal infection

Ziyuan Wu1, Nguyen Tran Nam Tien2, Björn Klabunde1

  • 1Comparative Pediatrics, Department of Veterinary and Animal Sciences, University of Copenhagen, Frederiksberg, Denmark.

EMBO Molecular Medicine
|June 8, 2026
PubMed

Insights

Nutritional strategies boosting the tricarboxylic acid (TCA) cycle improve newborn infection defense. Substituting glucose with galactose or amino acids in parenteral nutrition enhances pathogen clearance and prevents sepsis in vulnerable infants.

Area of Science:

  • Neonatal Medicine
  • Metabolic Research
  • Immunology

Background:

  • Preterm infants face high infection risks, with limited therapies beyond antibiotics.
  • The interplay between nutrition, energy metabolism, and neonatal immune defense is not well understood.

Purpose of the Study:

  • To investigate the role of tricarboxylic acid (TCA) cycle metabolites in neonatal infection outcomes.
  • To explore nutritional strategies that modulate TCA cycle activity for improved infection defense.

Main Methods:

  • Analysis of plasma TCA metabolites in a human birth cohort (n=700).
  • Utilized a piglet neonatal sepsis model to assess hepatic TCA cycle activity and survival.
  • Investigated the effects of substituting glucose with galactose or amino acids in parenteral nutrition.

Main Results:

  • Elevated plasma TCA metabolites correlated with reduced infection and inflammation in infants.
  • Sustained hepatic TCA cycle activity was linked to survival in a neonatal sepsis model.
  • Galactose or amino acid-based parenteral nutrition improved pathogen clearance, glucose homeostasis, and prevented lethal sepsis.

Conclusions:

  • Tricarboxylic acid (TCA) cycle metabolites are key regulators of early-life infection outcomes.
  • Nutritional modulation of the TCA cycle offers a promising therapeutic strategy for neonatal infections.
  • Targeting hepatic energy metabolism can enhance neonatal host defense against sepsis and reduce organ injury.

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