ArticleThe Journal of biological chemistry2009
Streptolysin O promotes group A Streptococcus immune evasion by accelerated macrophage apoptosis.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
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Who cites it
107 citing papers in PubMed, 180 citations in OpenAlex.
- Group A Streptococcus secreted esterase hydrolyzes platelet-activating factor to impede neutrophil recruitment and facilitate innate immune evasion.PLoS pathogens · 2012Trial
- Synergetic attenuated inflammatory response and increased apoptosis confer high pathogenicity ofVirulence · 2026Article
- Lysosomal permeabilization by Group AInfection and immunity · 2026Article
- Molecular characterization of covRS mutations in M1FEBS open bio · 2026Article
- Group A Streptococcal Virulence Factors and Vaccine Development-An Update.Microorganisms · 2026Review
- <italic>Streptococcus pyogenes</italic> Infection and CD4Journal of innate immunity · 2026Article
- Host-response trajectories in necrotizing fasciitis: host-pathogen interactions, immune evasion, and immunoparalysis.Frontiers in cellular and infection microbiology · 2026Review
- NasalJournal of inflammation research · 2026Article
- Lysosomal permeabilization by Group AbioRxiv : the preprint server for biology · 2025Article
- The burden of group AiScience · 2025Review
- The intricate pathogenicity of Group AVirulence · 2024Review
- Dissemination of pathogenic bacteria is reinforced by a MARTX toxin effector duet.Nature communications · 2024Article
- EmergentInfection and immunity · 2024Article
- Group AInfection and immunity · 2024Article
- Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024Review
- Streptolysin S is required for Streptococcus pyogenes nasopharyngeal and skin infection in HLA-transgenic mice.PLoS pathogens · 2024Article
- Reduced interleukin-18 secretion by human monocytic cells in response to infections with hyper-virulent Streptococcus pyogenes.Journal of biomedical science · 2024Article
- Group A Streptococcus strains causing meningitis without distinct invasive phenotype.MicrobiologyOpen · 2024Article
- StreptococcusVirulence · 2023Article
- Elucidation of independently modulated genes inmSystems · 2023Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Group A Streptococcus (GAS) is a leading human bacterial pathogen capable of producing invasive infections even in previously healthy individuals. As frontline components of host innate defense, macrophages play a key role in control and clearance of GAS infections. We find GAS induces rapid, dose-dependent apoptosis of primary and cultured macrophages and neutrophils. The cell death pathway involves apoptotic caspases, is partly dependent on caspase-1, and requires GAS internalization by the phagocyte. Analysis of GAS virulence factor mutants, heterologous expression, and purified toxin studies identified the pore-forming cytolysin streptolysin O (SLO) as necessary and sufficient for the apoptosis-inducing phenotype. SLO-deficient GAS mutants induced less macrophage apoptosis in vitro and in vivo, allowed macrophage cytokine secretion, and were less virulent in a murine systemic infection model. Ultrastructural evidence of mitochondrial membrane remodeling, coupled with loss of mitochondrial depolarization and cytochrome c release, suggests a direct attack of the toxin initiates the intrinsic apoptosis pathway. A general caspase inhibitor blocked SLO-induced apoptosis and enhanced macrophage killing of GAS. We conclude that accelerated, caspase-dependent macrophage apoptosis induced by the pore-forming cytolysin SLO contributes to GAS immune evasion and virulence.
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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.