ArticleNature communications2025
Oxidative phosphorylation is a key feature of neonatal monocyte immunometabolism promoting myeloid differentiation after birth.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Plasticity of the infant immune system during the perinatal period.Nature reviews. Immunology · 2026Review
- Time to rethink prevention of neonatal group B streptococcal disease.Seminars in immunopathology · 2026Review
- BCG vaccination potentiates oxidative phosphorylation in neonatal myeloid-derived suppressor cells.FEBS open bio · 2026Article
- Multi-omics insights into immunometabolic dysregulation in neonatal sepsis for precision medicine.Molecular biology reports · 2026Review
- Immune development in early life.Nature immunology · 2026Review
- Monocyte/macrophage-mediated trained immunity in disease prevention and immunotherapy.Bioactive materials · 2026Review
- A scoping review on the possible immunometabolic properties of the furan fatty acid metabolite 3-carboxy-4-methyl-5-propyl-2-furanpropionic acid.The American journal of clinical nutrition · 2025Article
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Corrections and comments
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Authors and funding
24 authors.
Funding
Abstract
Neonates primarily rely on innate immune defense, yet their inflammatory responses are usually restricted compared to adults. This is controversially interpreted as a sign of immaturity or essential programming, increasing or decreasing the risk of sepsis, respectively. Here, combined transcriptomic, metabolic, and immunological studies in monocytes of healthy individuals reveal an inverse ontogenetic shift in metabolic pathway activities with increasing age. Neonatal monocytes are characterized by enhanced oxidative phosphorylation supporting ongoing myeloid differentiation. This phenotype is gradually replaced during early childhood by increasing glycolytic activity fueling the inflammatory responsiveness. Microbial stimulation shifts neonatal monocytes to an adult-like metabolism, whereas ketogenic diet in adults mimicking neonatal ketosis cannot revive a neonate-like metabolism. Our findings disclose hallmarks of innate immunometabolism during healthy postnatal immune adaptation and suggest that premature activation of glycolysis in neonates might increase their risk of sepsis by impairing myeloid differentiation and promoting hyperinflammation.
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Registered trials
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