ArticleInfection and immunity2005
Role of NADase in virulence in experimental invasive group A streptococcal infection.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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.
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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
42 citing papers in PubMed, 65 citations in OpenAlex.
- Immunomodulating Enzymes fromMicroorganisms · 2024Review
- Interplay between human STING genotype and bacterial NADase activity regulates inter-individual disease variability.Nature communications · 2023Article
- Structural basis underlying the synergism of NADase and SLO during group A Streptococcus infection.Communications biology · 2023Article
- Products of gut microbial Toll/interleukin-1 receptor domain NADase activities in gnotobiotic mice and Bangladeshi children with malnutrition.Cell reports · 2022Article
- Diversity and prevalence of type VI secretion system effectors in clinicalFrontiers in microbiology · 2022Article
- Streptococcal Toxic Shock Syndrome Induced by Group A Streptococcus with the emm28 Genotype That Developed after a Uterine Cancer Test.Internal medicine (Tokyo, Japan) · 2021Article
- Streptolysin O concentration and activity is central to in vivo phenotype and disease outcome in Group A Streptococcus infection.Scientific reports · 2021Article
- Population Genomics ofmSystems · 2021Article
- TheJournal of bacteriology · 2021Article
- Tissue Tropism in Streptococcal Infection: Wild-Type M1T1 Group AInfection and immunity · 2019Article
- Integrated analysis of population genomics, transcriptomics and virulence provides novel insights into Streptococcus pyogenes pathogenesis.Nature genetics · 2019Article
- Gene fitness landscape of group A streptococcus during necrotizing myositis.The Journal of clinical investigation · 2019Article
- Tryptophan Metabolism: A Versatile Area Providing Multiple Targets for Pharmacological Intervention.Egyptian journal of basic and clinical pharmacology · 2019Article
- The Secreted Virulence Factor NADase of Group AFrontiers in immunology · 2019Article
- Streptolysin O derived from Streptococcus pyogenes inhibits RANKL‑induced osteoclastogenesis through the NF‑κB signaling pathway.Molecular medicine reports · 2019Article
- NAD-Glycohydrolase Depletes Intracellular NADFrontiers in microbiology · 2018Article
- Requirement and Synergistic Contribution of Platelet-Activating Factor Acetylhydrolase Sse and Streptolysin S to Inhibition of Neutrophil Recruitment and Systemic Infection by HypervirulentInfection and immunity · 2017Article
- Binding of NADmBio · 2017Article
- Article
- Contribution of Secreted NADase and Streptolysin O to the Pathogenesis of Epidemic Serotype M1 Streptococcus pyogenes Infections.The American journal of pathology · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Group A streptococci (GAS) produce several exoproteins that are thought to contribute to the pathogenesis of human infection. Two such proteins, streptolysin O (SLO) and NAD(+)-glycohydrolase (NADase), have been shown to interact functionally as a compound signaling toxin. When GAS are bound to the surface of epithelial cells in vitro, SLO forms pores in the cell membrane and delivers NADase to the epithelial cell cytoplasm. In vitro, intoxication of keratinocytes with NADase is associated with cytotoxic effects and induction of apoptosis; however, the importance of NADase during infection of an animal host has not been established. We employed isogenic GAS mutants to assess the contribution of NADase activity to GAS virulence in vivo using mouse models of invasive soft-tissue infection and septicemia. In both models, mutant GAS that lacked NADase activity were significantly attenuated for virulence compared with the isogenic wild-type parent, confirming an important role for NADase in the infection of a host animal. A double mutant lacking SLO and NADase activity had an intermediate virulence phenotype, consistent with the hypothesis that SLO evokes a protective innate immune response. We conclude that NADase and SLO together enhance GAS virulence in vivo.
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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.