ArticleCell host & microbe2015
Synergistic Action of Staphylococcus aureus α-Toxin on Platelets and Myeloid Lineage Cells Contributes to Lethal Sepsis.
Article in Cell host & microbe, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
82 citing papers in PubMed, 107 citations in OpenAlex.
- Platelet homeostasis and heterogeneity in inflammation and sepsis: mechanisms, biological effects, and clinical potential.Cell communication and signaling : CCS · 2026Review
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- Multivalent nanobodies for potent and broad neutralization of Staphylococcus aureus toxins.Nature communications · 2026Article
- Neonatal Sepsis-Induced Coagulopathy in the Light of Developmental Hemostasis: Friend or Foe?Medicina (Kaunas, Lithuania) · 2026Review
- The Clinical View of Sepsis-Associated AKI: How Basic Science Can Help Solve This Problem.Seminars in nephrology · 2025Review
- Endothelial Glycocalyx Turnover in Vascular Health and Disease: Rethinking Endothelial Dysfunction.Annual review of biochemistry · 2025Review
- The type of pathogen is associated with organ failure and legacy dysfunction in patients with sepsis.Frontiers in immunology · 2025Article
- Platelets in infection: intrinsic roles and functional outcomes.Frontiers in immunology · 2025Review
- Bacterial interactions with platelets: defining key themes.Frontiers in immunology · 2025Review
- YjbH contributes toVirulence · 2024Article
- Enhanced Staphylococcus aureus protection by uncoupling of the α-toxin-ADAM10 interaction during murine neonatal vaccination.Nature communications · 2024Article
- A fungal metabolic regulator underlies infectious synergism during Candida albicans-Staphylococcus aureus intra-abdominal co-infection.Nature communications · 2024Article
- Engineered Extracellular Vesicles Driven by Erythrocytes Ameliorate Bacterial Sepsis by Iron Recycling, Toxin Clearing and Inflammation Regulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The role of Staphylococcus aureus quorum sensing in cutaneous and systemic infections.Inflammation and regeneration · 2024Review
- Platelet P2YBritish journal of pharmacology · 2024Review
- The role of platelets in sepsis: A review.Biomolecules & biomedicine · 2024Review
- Necroptosis in bacterial infections.Frontiers in immunology · 2024Review
- Endothelial ADAM10 utilization defines a molecular pathway of vascular injury in mice with bacterial sepsis.The Journal of clinical investigation · 2023Article
- Staphylococcus aureus α-toxin impairs early neutrophil localization via electrogenic disruption of store-operated calcium entry.Cell reports · 2023Article
22 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
5 authors at 1 institution in 1 country.
Funding
Abstract
Multi-organ failure contributes to mortality in bacterial sepsis. Platelet and immune cell activation contribute to organ injury during sepsis, but the mechanisms by which bacterial virulence factors initiate these responses remain poorly defined. We demonstrate that during lethal sepsis, Staphylococcus aureus α-toxin simultaneously alters platelet activation and promotes neutrophil inflammatory signaling through interactions with its cellular receptor ADAM10. Platelet intoxication prevents endothelial barrier repair and facilitates formation of injurious platelet-neutrophil aggregates, contributing to lung and liver injury that is mitigated by ADAM10 deletion on platelets and myeloid lineage cells. While platelet- or myeloid-specific ADAM10 knockout does not alter sepsis mortality, double-knockout animals are highly protected. These results define a pathway by which a single bacterial toxin utilizes a widely expressed receptor to coordinate progressive, multi-organ disease in lethal sepsis. As an expression-enhancing ADAM10 polymorphism confers susceptibility to severe human sepsis, these studies highlight the importance of understanding molecular host-microbe interactions.
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What OpenQuestion holds
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.