ArticleThe Journal of biological chemistry2011
Streptolysin S contributes to group A streptococcal translocation across an epithelial barrier.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 97 citations in OpenAlex.
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- Global spread of Streptococcus pyogenes A genomics-supported narrative review.FEMS microbiology reviews · 2025Review
- Respiratory tract barrier dysfunction in viral-bacterial co-infection cases.The Japanese dental science review · 2024Review
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- 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
- Identification of distinct impacts of CovS inactivation on the transcriptome of acapsular group A streptococci.mSystems · 2023Article
- Streptolysin S induces pronounced calcium-ion influx-dependent expression of immediate early genes encoding transcription factors.Scientific reports · 2023Article
- Direct and indirect effects of pathogenic bacteria on the integrity of intestinal barrier.Therapeutic advances in gastroenterology · 2023Review
- Glaesserella parasuis serotype 5 breaches the porcine respiratory epithelial barrier by inducing autophagy and blocking the cell membrane Claudin-1 replenishment.PLoS pathogens · 2022Article
- Mechanism of Action of Ribosomally Synthesized and Post-Translationally Modified Peptides.Chemical reviews · 2022Review
- The group AInfectious microbes & diseases · 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
- GP96 Drives Exacerbation of Secondary Bacterial Pneumonia following Influenza A Virus Infection.mBio · 2021Article
- Intracellular Group AmBio · 2021Article
- Playing With Fire: Proinflammatory Virulence Mechanisms of Group AFrontiers in cellular and infection microbiology · 2021Review
- Plasma Protein Layer Concealment ProtectsFrontiers in cellular and infection microbiology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group A Streptococcus pyogenes (GAS) is a human pathogen that causes local suppurative infections and severe invasive diseases. Systemic dissemination of GAS is initiated by bacterial penetration of the epithelial barrier of the pharynx or damaged skin. To gain insight into the mechanism by which GAS penetrates the epithelial barrier, we sought to identify both bacterial and host factors involved in the process. Screening of a transposon mutant library of a clinical GAS isolate recovered from an invasive episode allowed identification of streptolysin S (SLS) as a novel factor that facilitates the translocation of GAS. Of note, the wild type strain efficiently translocated across the epithelial monolayer, accompanied by a decrease in transepithelial electrical resistance and cleavage of transmembrane junctional proteins, including occludin and E-cadherin. Loss of integrity of intercellular junctions was inhibited after infection with a deletion mutant of the sagA gene encoding SLS, as compared with those infected with the wild type strain. Interestingly, following GAS infection, calpain was recruited to the plasma membrane along with E-cadherin. Moreover, bacterial translocation and destabilization of the junctions were partially inhibited by a pharmacological calpain inhibitor or genetic interference with calpain. Our data indicate a potential function of SLS that facilitates GAS invasion into deeper tissues via degradation of epithelial intercellular junctions in concert with the host cysteine protease calpain.
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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.