ArticleFrontiers in immunology2015
Streptolysin O Rapidly Impairs Neutrophil Oxidative Burst and Antibacterial Responses to Group A Streptococcus.
Article in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 95 citations in OpenAlex.
- A fully human streptolysin O-neutralizing monoclonal antibody improves survival in a murine model of group A streptococcus necrotizing soft tissue infection.Antimicrobial agents and chemotherapy · 2026Article
- Mechanisms underlying pyogenic bacterial infections of the skin.Archives of microbiology · 2026Review
- Rational selection of antigenic targets for Group A Streptococcus vaccine: updates, challenges and opportunities.NPJ vaccines · 2026Review
- Bacterial pore-forming toxins: mechanisms and implications for host immunity.Bioscience reports · 2026Review
- Group A Streptococcal Virulence Factors and Vaccine Development-An Update.Microorganisms · 2026Review
- Host-response trajectories in necrotizing fasciitis: host-pathogen interactions, immune evasion, and immunoparalysis.Frontiers in cellular and infection microbiology · 2026Review
- <italic>Streptococcus pyogenes</italic> Infection and CD4Journal of innate immunity · 2026Article
- Mechanisms and immune crosstalk of neutrophil extracellular traps in response to infection.mBio · 2025Review
- Candida albicans aspartyl protease (Sap6) inhibits neutrophil function via a "Trojan horse" mechanism.Scientific reports · 2025Article
- Uncommon Systemic Manifestation of Group A Beta-Hemolytic Streptococcus in a Middle-Aged Woman: A Case Report.Cureus · 2025Article
- The intricate pathogenicity of Group AVirulence · 2024Review
- Streptolysin O accelerates the conversion of plasminogen to plasmin.Nature communications · 2024Article
- Multimodal Mass Spectrometry Identifies a Conserved Protective Epitope inAnalytical chemistry · 2024Article
- Story of Pore-Forming Proteins from Deadly Disease-Causing Agents to Modern Applications with Evolutionary Significance.Molecular biotechnology · 2024Review
- Development and characterization of a hemolysis inhibition assay to determine functionality of anti-Streptolysin O antibodies in human sera.Journal of immunological methods · 2024Article
- Streptolysin S is required for Streptococcus pyogenes nasopharyngeal and skin infection in HLA-transgenic mice.PLoS pathogens · 2024Article
- Neutrophil extracellular traps in bacterial infections and evasion strategies.Frontiers in immunology · 2024Review
- Neutrophil Extracellular Traps in Tumors and Potential Use of Traditional Herbal Medicine Formulations for Its Regulation.International journal of nanomedicine · 2024Review
- Correlation of Streptococcus agalactiae concentration on immune system and effective dose of inactivated vaccine for Chitralada 3 strain Nile tilapia (Oreochromis niloticus) in Thailand.BMC veterinary research · 2023Article
- Pathogenesis, epidemiology and control of Group A Streptococcus infection.Nature reviews. Microbiology · 2023Review
4 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Group A Streptococcus (GAS) causes a wide range of human infections, ranging from simple pharyngitis to life-threatening necrotizing fasciitis and toxic shock syndrome. A globally disseminated clone of M1T1 GAS has been associated with an increase in severe, invasive GAS infections in recent decades. The secreted GAS pore-forming toxin streptolysin O (SLO), which induces eukaryotic cell lysis in a cholesterol-dependent manner, is highly upregulated in the GAS M1T1 clone during bloodstream dissemination. SLO is known to promote GAS resistance to phagocytic clearance by neutrophils, a critical first element of host defense against invasive bacterial infection. Here, we examine the role of SLO in modulating specific neutrophil functions during their early interaction with GAS. We find that SLO at subcytotoxic concentrations and early time points is necessary and sufficient to suppress neutrophil oxidative burst, in a manner reversed by free cholesterol and anti-SLO blocking antibodies. In addition, SLO at subcytotoxic concentrations blocked neutrophil degranulation, interleukin-8 secretion and responsiveness, and elaboration of DNA-based neutrophil extracellular traps, cumulatively supporting a key role for SLO in GAS resistance to immediate neutrophil killing. A non-toxic SLO derivate elicits protective immunity against lethal GAS challenge in a murine infection model. We conclude that SLO exerts a novel cytotoxic-independent function at early stages of invasive infections (<30 min), contributing to GAS escape from neutrophil clearance.
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