ArticleCell reports2023
Staphylococcus aureus α-toxin impairs early neutrophil localization via electrogenic disruption of store-operated calcium entry.
Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 9 citations in OpenAlex.
- TLR7/9 and type I interferon signaling reprogram neutrophil NET responses and impair antibacterial defense in systemic lupus erythematosus.Cell press blue · 2026Article
- Adipocyte-derived LTB4 programs human NKG2AJournal for immunotherapy of cancer · 2026Article
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- Mechanisms underlying pyogenic bacterial infections of the skin.Archives of microbiology · 2026Review
- Tunable TriPcides suppress virulence factor secretion duringScience advances · 2026Article
- Arachidonic acid availability controls neutrophil swarm initiation and scaling.bioRxiv : the preprint server for biology · 2026Article
- Increased Bacterial Load per Neutrophil Reduces Intracellular Killing Capacity.Journal of innate immunity · 2026Article
- A TLR7/9-IFNα-LDHB axis drives vital NET release and compromises antibacterial defense in lupus.bioRxiv : the preprint server for biology · 2025Article
- STIM1/2 maintain signaling competence at ER-PM contact sites during neutrophil spreading.The Journal of cell biology · 2025Article
- Enhanced Staphylococcus aureus protection by uncoupling of the α-toxin-ADAM10 interaction during murine neonatal vaccination.Nature communications · 2024Article
- Self-extinguishing relay waves enable homeostatic control of human neutrophil swarming.Developmental cell · 2024Article
- TRPA1 InfluencesInternational journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
The pore-forming S. aureus α-toxin (Hla) contributes to virulence and disease pathogenesis. While high concentrations of toxin induce cell death, neutrophils exhibit relative resistance to lysis, suggesting that the action of Hla may not be solely conferred by lytic susceptibility. Using intravital microscopy, we observed that Hla disrupts neutrophil localization and clustering early in infection. Hla forms a narrow, ion-selective pore, suggesting that Hla may dysregulate calcium or other ions to impair neutrophil function. We found that sub-lytic Hla did not permit calcium influx but caused rapid membrane depolarization. Depolarization decreases the electrogenic driving force for calcium, and concordantly, Hla suppressed calcium signaling in vitro and in vivo and calcium-dependent leukotriene B4 (LTB4) production, a key mediator of neutrophil clustering. Thus, Hla disrupts the early patterning of the neutrophil response to infection, in part through direct impairment of neutrophil calcium signaling. This early mis-localization of neutrophils may contribute to establishment of 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.