ArticleThe Journal of biological chemistry2014
Bacterial RTX toxins allow acute ATP release from human erythrocytes directly through the toxin pore.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 57 citations in OpenAlex.
- Erythrocytes as Active Regulators of Blood Flow: A Brief Overview.Advances in experimental medicine and biology · 2026Review
- The Mitochondrial Permeability Transition Pore in Platelets: Mechanisms, Physiological Roles, and Therapeutic Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- Purinergic Receptor Antagonists Inhibit Hemolysis Induced byPathogens (Basel, Switzerland) · 2024Article
- Adenosine triphosphate induced cell death: Mechanisms and implications in cancer biology and therapy.World journal of clinical oncology · 2023Review
- Nucleotide receptors mediate protection against neonatal sepsis and meningitis caused by alpha-hemolysin expressing Escherichia coli K1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Review
- Leukotoxin (LtxA/Leukothera) induces ATP expulsion via pannexin-1 channels and subsequent cell death in malignant lymphocytes.Scientific reports · 2021Article
- P2RX7 at the Host-Pathogen Interface of Infectious Diseases.Microbiology and molecular biology reviews : MMBR · 2021Review
- Role of astroglial Connexin 43 in pneumolysin cytotoxicity and during pneumococcal meningitis.PLoS pathogens · 2020Article
- Prevention of P2 Receptor-Dependent Thrombocyte Activation by Pore-Forming Bacterial Toxins Improves Outcome in A Murine Model of Urosepsis.International journal of molecular sciences · 2020Article
- Extracellular ATP as an Inter-Kingdom Signaling Molecule: Release Mechanisms by Bacteria and Its Implication on the Host.International journal of molecular sciences · 2020Review
- Aggregatibacter actinomycetemcomitans leukotoxin: From mechanism to targeted anti-toxin therapeutics.Molecular oral microbiology · 2020Review
- Review
- Potential Role of Extracellular ATP Released by Bacteria in Bladder Infection and Contractility.mSphere · 2019Article
- P2XPurinergic signalling · 2019Article
- Comparative Genome Analysis of UropathogenicFrontiers in cellular and infection microbiology · 2019Article
- Erythrocyte P2XCritical care (London, England) · 2018Article
- Human erythrocytes release ATP by a novel pathway involving VDAC oligomerization independent of pannexin-1.Scientific reports · 2018Article
- Research articleHemolysis in human erythrocytes by Clostridium perfringens epsilon toxin requires activation of P2 receptors.Virulence · 2018Article
- P2X-Receptor Antagonists Inhibit the Interaction of S. aureus Hemolysin A with Membranes.Toxins · 2017Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ATP is as an extracellular signaling molecule able to amplify the cell lysis inflicted by certain bacterial toxins including the two RTX toxins α-hemolysin (HlyA) from Escherichia coli and leukotoxin A (LtxA) from Aggregatibacter actinomycetemcomitans. Inhibition of P2X receptors completely blocks the RTX toxin-induced hemolysis over a larger concentration range. It is, however, at present not known how the ATP that provides the amplification is released from the attacked cells. Here we show that both HlyA and LtxA trigger acute release of ATP from human erythrocytes that preceded and were not caused by cell lysis. This early ATP release did not occur via previously described ATP-release pathways in the erythrocyte. Both HlyA and LtxA were capable of triggering ATP release in the presence of the pannexin 1 blockers carbenoxolone and probenecid, and the HlyA-induced ATP release was found to be similar in erythrocytes from pannexin 1 wild type and knock-out mice. Moreover, the voltage-dependent anion channel antagonist TRO19622 had no effect on ATP release by either of the toxins. Finally, we showed that both HlyA and LtxA were able to release ATP from ATP-loaded lipid (1-palmitoyl-2-oleoyl-phosphatidylcholine) vesicles devoid of any erythrocyte channels or transporters. Again we were able to show that this happened in a non-lytic fashion, using calcein-containing vesicles as controls. These data show that both toxins incorporate into lipid vesicles and allow ATP to be released. We suggest that both toxins cause acute ATP release by letting ATP pass the toxin pores in both human erythrocytes and artificial membranes.
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