ArticleThe Journal of cell biology2001
alpha-Toxin is a mediator of Staphylococcus aureus-induced cell death and activates caspases via the intrinsic death pathway independently of death receptor signaling.
Article in The Journal of cell biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 192 citations in OpenAlex.
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- Cell Death and Infection: Implications for Host and Microbe.Advances in experimental medicine and biology · 2025Review
- Enhancing the Cytotoxicity and Apoptotic Efficacy of Parasporin-2-Derived Variants (Mpp46Aa1) on Cancer Cell Lines.Toxins · 2024Article
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- State of the Art on the Role ofMicroorganisms · 2024Review
- In Vivo Detection ofInternational journal of biomedical imaging · 2024Article
- Mitochondrial Dysfunction in Bacterial Infections.Pathogens (Basel, Switzerland) · 2023Review
- Exploring the Role ofToxins · 2022Review
- Chronic Rhinosinusitis,Biomedicines · 2022Review
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- Comparison of Antivirulence Activities of Black Ginseng against Methicillin-ResistantAntibiotics (Basel, Switzerland) · 2021Article
- Phosphatidylinositol-specific phospholipase C enhances epidermal penetration by Staphylococcus aureus.Scientific reports · 2020Article
- SuicidalPathogens (Basel, Switzerland) · 2020Article
- Selective Host Cell Death byFrontiers in immunology · 2020Review
- Manipulation of Autophagy and Apoptosis Facilitates Intracellular Survival ofFrontiers in immunology · 2020Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infections with Staphylococcus aureus, a common inducer of septic and toxic shock, often result in tissue damage and death of various cell types. Although S. aureus was suggested to induce apoptosis, the underlying signal transduction pathways remained elusive. We show that caspase activation and DNA fragmentation were induced not only when Jurkat T cells were infected with intact bacteria, but also after treatment with supernatants of various S. aureus strains. We also demonstrate that S. aureus-induced cell death and caspase activation were mediated by alpha-toxin, a major cytotoxin of S. aureus, since both events were abrogated by two different anti-alpha-toxin antibodies and could not be induced with supernatants of an alpha-toxin-deficient S. aureus strain. Furthermore, alpha-toxin-induced caspase activation in CD95-resistant Jurkat sublines lacking CD95, Fas-activated death domain, or caspase-8 but not in cells stably expressing the antiapoptotic protein Bcl-2. Together with our finding that alpha-toxin induces cytochrome c release in intact cells and, interestingly, also from isolated mitochondria in a Bcl-2-controlled manner, our results demonstrate that S. aureus alpha-toxin triggers caspase activation via the intrinsic death pathway independently of death receptors. Hence, our findings clearly define a signaling pathway used in S. aureus-induced cytotoxicity and may provide a molecular rationale for future therapeutic interventions in bacterial infections.
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