ArticleInfection and immunity2015
Streptolysin S Promotes Programmed Cell Death and Enhances Inflammatory Signaling in Epithelial Keratinocytes during Group A Streptococcus Infection.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- An in-depth review on antimicrobial efficacy of melittin in vivo.World journal of microbiology & biotechnology · 2026Review
- Article
- Characterization of a novelmBio · 2025Article
- 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 proinflammatory cytokine expression in calcium ion-influx-dependent manner.Current research in microbial sciences · 2024Article
- StreptococcusVirulence · 2023Article
- Streptolysin S induces pronounced calcium-ion influx-dependent expression of immediate early genes encoding transcription factors.Scientific reports · 2023Article
- Pathogenesis, epidemiology and control of Group A Streptococcus infection.Nature reviews. Microbiology · 2023Review
- Streptococcal peptides and their roles in host-microbe interactions.Frontiers in cellular and infection microbiology · 2023Review
- AssessingFrontiers in cellular and infection microbiology · 2022Article
- Streptolysin S targets the sodium-bicarbonate cotransporter NBCn1 to induce inflammation and cytotoxicity in human keratinocytes during Group A Streptococcal infection.Frontiers in cellular and infection microbiology · 2022Article
- Distinct Group BInfection and immunity · 2021Article
- Streptococcus pyogenes infects human endometrium by limiting the innate immune response.The Journal of clinical investigation · 2021Article
- Immunization With a Secreted Esterase Protects Mice Against Multiple Serotypes (M1, M3, and M28) of Group AFrontiers in microbiology · 2020Article
- Modulation of Death and Inflammatory Signaling in Decidual Stromal Cells following Exposure to Group BInfection and immunity · 2019Article
- Streptococcal sagA activates a proinflammatory response in mast cells by a sublytic mechanism.Cellular microbiology · 2019Article
- Streptolysin S induces mitochondrial damage and macrophage death through inhibiting degradation of glycogen synthase kinase-3β in Streptococcus pyogenes infection.Scientific reports · 2019Article
- The Pathogenesis OfInfection and drug resistance · 2019Article
- Toxins and Superantigens of Group A Streptococci.Microbiology spectrum · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Streptococcus pyogenes, or group A Streptococcus (GAS), is a pathogen that causes a multitude of human diseases from pharyngitis to severe infections such as toxic shock syndrome and necrotizing fasciitis. One of the primary virulence factors produced by GAS is the peptide toxin streptolysin S (SLS). In addition to its well-recognized role as a cytolysin, recent evidence has indicated that SLS may influence host cell signaling pathways at sublytic concentrations during infection. We employed an antibody array-based approach to comprehensively identify global host cell changes in human epithelial keratinocytes in response to the SLS toxin. We identified key SLS-dependent host responses, including the initiation of specific programmed cell death and inflammatory cascades with concomitant downregulation of Akt-mediated cytoprotection. Significant signaling responses identified by our array analysis were confirmed using biochemical and protein identification methods. To further demonstrate that the observed SLS-dependent host signaling changes were mediated primarily by the secreted toxin, we designed a Transwell infection system in which direct bacterial attachment to host cells was prevented, while secreted factors were allowed access to host cells. The results using this approach were consistent with our direct infection studies and reveal that SLS is a bacterial toxin that does not require bacterial attachment to host cells for activity. In light of these findings, we propose that the production of SLS by GAS during skin infection promotes invasive outcomes by triggering programmed cell death and inflammatory cascades in host cells to breach the keratinocyte barrier for dissemination into deeper tissues.
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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.