ArticleNature immunology2017
S100-alarmin-induced innate immune programming protects newborn infants from sepsis.
Article in Nature immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 106 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
106 citing papers in PubMed, 159 citations in OpenAlex.
- The gut-lung axis in early life: microbiome-associated mechanisms and clinical relevance.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Trained immunity modulators: A new frontier in immunoregulation and disease intervention.Journal of advanced research · 2026Review
- Population-specific heterogeneity in ontogeny of the broadly-conserved blood transcriptional program during the first week of life.Nature communications · 2026Article
- Neonatal intensive care unit exposures reprogram microbiome-metabolome trajectories and modulate host calprotectin in preterm infants: a longitudinal multi-omics study.NPJ biofilms and microbiomes · 2026Article
- S100-alarmins, antenatal corticosteroids and the risk of late-onset sepsis in preterm infants: A prospective cohort study.PloS one · 2026Article
- Interaction BetweenCurrent pharmaceutical biotechnology · 2026Review
- Article
- Reading of human acute immune dynamics in omicron SARS-CoV-2 breakthrough infection.Emerging microbes & infections · 2025Article
- Microbiome in heritage: how maternal microbiome transmission impacts next generation health.Microbiome · 2025Review
- Maternal emulsifier consumption alters the offspring early-life microbiota and goblet cell function leading to long-lasting diseases susceptibility.Nature communications · 2025Article
- Review
- FXR protects against neonatal sepsis by enhancing the immunosuppressive function of MDSCs.Cellular & molecular immunology · 2025Article
- Innate immune training in the neonatal response to sepsis.Molecular medicine (Cambridge, Mass.) · 2025Article
- Oxidative phosphorylation is a key feature of neonatal monocyte immunometabolism promoting myeloid differentiation after birth.Nature communications · 2025Article
- Differences in immune cells and gene expression in human milk by parity on integrated scRNA sequencing.Clinical and experimental pediatrics · 2025Article
- Exploring Differentially Methylated Genes among Preterm Birth and Full-Term Birth.Lifestyle genomics · 2025Article
- Postnatal supplementation with alarmins S100a8/a9 ameliorates malnutrition-induced neonate enteropathy in mice.Nature communications · 2024Article
- Risk assessment with gene expression markers in sepsis development.Cell reports. Medicine · 2024Article
- Neuropilin-1Cellular & molecular immunology · 2024Article
- Article
46 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
25 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The high risk of neonatal death from sepsis is thought to result from impaired responses by innate immune cells; however, the clinical observation of hyperinflammatory courses of neonatal sepsis contradicts this concept. Using transcriptomic, epigenetic and immunological approaches, we demonstrated that high amounts of the perinatal alarmins S100A8 and S100A9 specifically altered MyD88-dependent proinflammatory gene programs. S100 programming prevented hyperinflammatory responses without impairing pathogen defense. TRIF-adaptor-dependent regulatory genes remained unaffected by perinatal S100 programming and responded strongly to lipopolysaccharide, but were barely expressed. Steady-state expression of TRIF-dependent genes increased only gradually during the first year of life in human neonates, shifting immune regulation toward the adult phenotype. Disruption of this critical sequence of transient alarmin programming and subsequent reprogramming of regulatory pathways increased the risk of hyperinflammation and sepsis. Collectively these data suggest that neonates are characterized by a selective, transient microbial unresponsiveness that prevents harmful hyperinflammation in the delicate neonate while allowing for sufficient immunological protection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.