ArticleProceedings of the National Academy of Sciences of the United States of America2009
Alpha-hemolysin from Escherichia coli uses endogenous amplification through P2X receptor activation to induce hemolysis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 131 citations in OpenAlex.
- RTX-family toxin EhxA drives morphological remodeling and thrombogenesis in RBCs during enterohemorrhagicScience advances · 2026Article
- Everything is everywhere but Escherichia coli adapts to different niches.The ISME journal · 2026Article
- Porin A and α/β-hydrolase are necessary and sufficient for hemolysis induced by Bartonella bacilliformis.Nature communications · 2025Article
- Activity of Peptides Modulating the Action of p2x Receptors: Focus on the p2x7 Receptor.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Purinergic Receptor Antagonists Inhibit Hemolysis Induced byPathogens (Basel, Switzerland) · 2024Article
- Uropathogen and host responses in pyelonephritis.Nature reviews. Nephrology · 2023Review
- Candidalysin Is the Hemolytic Factor ofToxins · 2022Article
- P2R Inhibitors Prevent Antibody-Mediated Complement Activation in an Animal Model of Neuromyelitis Optica : P2R Inhibitors Prevent Autoantibody Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Purinergic signaling is essential for full Psickle activation by hypoxia and by normoxic acid pH in mature human sickle red cells and in vitro-differentiated cultured human sickle reticulocytes.Pflugers Archiv : European journal of physiology · 2022Article
- 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
- Interactive Dynamics of Cell Volume and Cell Death in Human Erythrocytes Exposed to α-Hemolysin fromInternational journal of molecular sciences · 2022Article
- 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
- Clostridium perfringens epsilon toxin binds to erythrocyte MAL receptors and triggers phosphatidylserine exposure.Journal of cellular and molecular medicine · 2020Article
- NusG, an Ancient Yet Rapidly Evolving Transcription Factor.Frontiers in microbiology · 2020Review
- Article
- Review
16 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Escherichia coli is the dominant facultative bacterium in the normal intestinal flora. E. coli is, however, also responsible for the majority of serious extraintestinal infections. There are distinct serotypical differences between facultative and invasive E. coli strains. Invasive strains frequently produce virulence factors such as alpha-hemolysin (HlyA), which causes hemolysis by forming pores in the erythrocyte membrane. The present study reveals that this pore formation triggers purinergic receptor activation to mediate the full hemolytic action. Non-selective ATP-receptor (P2) antagonists (PPADS, suramin) and ATP scavengers (apyrase, hexokinase) concentration dependently inhibited HlyA-induced lysis of equine, murine, and human erythrocytes. The pattern of responsiveness to more selective P2-antagonists implies that both P2X(1) and P2X(7) receptors are involved in HlyA-induced hemolysis in all three species. In addition, our results also propose a role for the pore protein pannexin1 in HlyA-induced hemolysis, as non-selective inhibitors of this channel significantly reduced hemolysis in the three species. In conclusion, activation of P2X receptors and possibly also pannexins augment hemolysis induced by the bacterial toxin, HlyA. These findings potentially have clinical perspectives as P2 antagonists may ameliorate symptoms during sepsis with hemolytic bacteria.
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