ArticleScientific reports2019
Streptolysin S induces mitochondrial damage and macrophage death through inhibiting degradation of glycogen synthase kinase-3β in Streptococcus pyogenes infection.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Carbon metabolism and niche adaptation inmSphere · 2026Review
- RadicalJournal of the American Chemical Society · 2026Article
- Group A Streptococcal Virulence Factors and Vaccine Development-An Update.Microorganisms · 2026Review
- Global spread of Streptococcus pyogenes A genomics-supported narrative review.FEMS microbiology reviews · 2025Review
- Streptolysin S is required for Streptococcus pyogenes nasopharyngeal and skin infection in HLA-transgenic mice.PLoS pathogens · 2024Article
- Streptolysin S induces pronounced calcium-ion influx-dependent expression of immediate early genes encoding transcription factors.Scientific reports · 2023Article
- Bacterial pore-forming toxins.Microbiology (Reading, England) · 2022Article
- AssessingFrontiers in cellular and infection microbiology · 2022Article
- IL-33/ST2 Axis Plays a Protective Effect inInternational journal of molecular sciences · 2021Article
- Mitophagy and Innate Immunity in Infection.Molecules and cells · 2020Review
- Mechanisms of the Regulation and Dysregulation of Glucagon Secretion.Oxidative medicine and cellular longevity · 2020Review
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group A Streptococcus (GAS) infection is associated with a variety of human diseases. Previous studies indicate GAS infection leads to RAW264.7 cell death, but the mechanism is unclear. Here, analyzing the timing of reactive oxygen species (ROS) production and using mitochondrial ROS scavenger, we found the wild type GAS-induced RAW264.7 cell death was associated with mitochondrial ROS. The wild type GAS infection could activate glycogen synthase kinase-3β (GSK-3β). Inhibition of GSK-3β activity by lithium chloride or decreasing GSK-3β expression by lentivirus-mediated short hairpin RNA for GSK-3β could not only decrease the wild type GAS-induced mitochondrial ROS generation, mitochondria damage and cell death, but also reduced GAS intracellular replication. Streptolysin S (SLS), a GAS toxin, played the important role on GAS-induced macrophage death. Compared to the wild type GAS with its isogenic sagB mutant (SLS mutant)-infected macrophages, we found sagB mutant infection caused less mitochondrial ROS generation and cell death than those of the wild type GAS-infected ones. Furthermore, the sagB mutant, but not the wild type or the sagB-complementary mutant, could induce GSK-3β degradation via a proteasome-dependent pathway. These results suggest that a new mechanism of SLS-induced macrophage death was through inhibiting GSK-3β degradation and further enhancing mitochondrial damage.
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