ArticlePloS one2009
Staphylococcus aureus alpha-hemolysin activates the NLRP3-inflammasome in human and mouse monocytic cells.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 264 papers.
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Who cites it
264 citing papers in PubMed, 426 citations in OpenAlex.
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- Cytosolic CTH senses bacterial lipoproteins and drives noncanonical inflammasome activation.Nature immunology · 2026Article
- Sensing the spectrum: diverse stimuli for the NLRP3 inflammasome.Communications biology · 2026Review
- Differential sensitivity of leukocyte populations toInfection and immunity · 2026Article
- The toxic effects of α-hemolysin and β-hemolysin produced byFrontiers in immunology · 2026Review
- α-hemolysin polymorphisms in methicillin-resistantbioRxiv : the preprint server for biology · 2025Article
- Commensal Peptoniphilus harei induce activation of monocytes via TLR2/CD14 signalling in whole blood.Medical microbiology and immunology · 2025Article
- Overcoming Immune Evasion inACS infectious diseases · 2025Review
- Alpha hemolysin enhances the immune response by modulating dendritic cell differentiation via ADAM10-Notch signaling.Signal transduction and targeted therapy · 2025Article
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- Immune dysfunction during S. aureus biofilm-associated implant infections: opportunities for novel therapeutic strategies.NPJ biofilms and microbiomes · 2025Review
- Staphylococcus aureus promotes strain-dependent immunopathology during cutaneous leishmaniasis through induction of IL-1β.Cell reports · 2025Article
204 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Community Acquired Methicillin Resistant Staphylococcus aureus (CA-MRSA) causes severe necrotizing infections of the skin, soft tissues, and lungs. Staphylococcal alpha-hemolysin is an essential virulence factor in mouse models of CA-MRSA necrotizing pneumonia. S. aureus alpha-hemolysin has long been known to induce inflammatory signaling and cell death in host organisms, however the mechanism underlying these signaling events were not well understood. Using highly purified recombinant alpha-hemolysin, we now demonstrate that alpha-hemolysin activates the Nucleotide-binding domain and leucine-rich repeat containing gene family, pyrin domain containing 3 protein (NLRP3)-inflammasome, a host inflammatory signaling complex involved in responses to pathogens and endogenous danger signals. Non-cytolytic mutant alpha-hemolysin molecules fail to elicit NLRP3-inflammasome signaling, demonstrating that the responses are not due to non-specific activation of this innate immune signaling system by bacterially derived proteins. In monocyte-derived cells from humans and mice, inflammasome assembly in response to alpha-hemolysin results in activation of the cysteine proteinase, caspase-1. We also show that inflammasome activation by alpha-hemolysin works in conjunction with signaling by other CA-MRSA-derived Pathogen Associated Molecular Patterns (PAMPs) to induce secretion of pro-inflammatory cytokines IL-1beta and IL-18. Additionally, alpha-hemolysin induces cell death in these cells through an NLRP3-dependent program of cellular necrosis, resulting in the release of endogenous pro-inflammatory molecules, like the chromatin-associated protein, High-mobility group box 1 (HMGB1). These studies link the activity of a major S. aureus virulence factor to a specific host signaling pathway. The cellular events linked to inflammasome activity have clear relevance to the disease processes associated with CA-MRSA including tissue necrosis and inflammation.
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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.