ArticleCell reports2017
Metabolic Stress Drives Keratinocyte Defenses against Staphylococcus aureus Infection.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
What it found
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Who cites it
61 citing papers in PubMed, 101 citations in OpenAlex.
- Infection-induced glucose starvation triggers NINJ1-dependent macrophage lysis and Candida escape.Nature communications · 2026Article
- Ketogenic diet synergistic reprogramming of both host and microbiome promotes tissue regeneration.bioRxiv : the preprint server for biology · 2026Article
- Metabolic adaptation drives self-organization during skin organoid morphogenesis.Nature communications · 2026Article
- Fungal infection drives metabolic reprogramming in epithelial cells via aerobic glycolysis and an alternative TCA cycle shunt.Science advances · 2026Article
- Comprehensive analysis of human keratinocyte interactions withVirulence · 2025Article
- Staphylococcus aureus accessory gene regulator quorum-sensing system inhibits keratinocyte lipid enzymes and delays wound repair.The Journal of clinical investigation · 2025Article
- Review
- Metabolic imprinting drives epithelial memory during mucosal fungal infection.bioRxiv : the preprint server for biology · 2025Article
- The flux of energy in critical illness and the obesity paradox.Physiological reviews · 2025Review
- Circadian metabolic adaptations to infections.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Implant-DerivedAntibiotics (Basel, Switzerland) · 2025Article
- Skin microbiota and diabetic foot ulcers.Frontiers in microbiology · 2025Review
- The role of glucose metabolism in wound healing: an overview.Burns & trauma · 2025Review
- Post-translational toxin modification by lactate controls Staphylococcus aureus virulence.Nature communications · 2024Article
- Yersinia infection induces glucose depletion and AMPK-dependent inhibition of pyroptosis in mice.Nature microbiology · 2024Article
- The Complex Intracellular Lifecycle ofInternational journal of molecular sciences · 2024Review
- ER-mitochondria association negatively affects wound healing by regulating NLRP3 activation.Cell death & disease · 2024Article
- Reduced Glycolysis and Cytotoxicity inInternational journal of molecular sciences · 2024Article
- Molecular Signaling and Metabolic Responses during the Interaction between Human Keratinocytes (HaCaT) and the DermatophyteJournal of fungi (Basel, Switzerland) · 2024Article
- IL-17A Orchestrates Reactive Oxygen Species/HIF1α-Mediated Metabolic Reprogramming in Psoriasis.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Human skin is commonly colonized and infected by Staphylococcus aureus. Exactly how these organisms are sensed by keratinocytes has not been clearly delineated. Using a combination of metabolic and transcriptomic methodologies, we found that S. aureus infection is sensed as a metabolic stress by the hypoxic keratinocytes. This induces HIF1α signaling, which promotes IL-1β production and stimulates aerobic glycolysis to meet the metabolic requirements of infection. We demonstrate that staphylococci capable of glycolysis, including WT and agr mutants, readily induce HIF1α responses. In contrast, Δpyk glycolytic mutants fail to compete with keratinocytes for their metabolic needs. Suppression of glycolysis using 2-DG blocked keratinocyte production of IL-1β in vitro and significantly exacerbated the S. aureus cutaneous infection in a murine model. Our data suggest that S. aureus impose a metabolic stress on keratinocytes that initiates signaling necessary to promote both glycolysis and the proinflammatory response to infection.
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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.