ArticleFrontiers in microbiology2014
The IL-8 protease SpyCEP is detrimental for Group A Streptococcus host-cells interaction and biofilm formation.
Article in Frontiers in microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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
9 citing papers in PubMed.
- Group A Streptococcus strains causing meningitis without distinct invasive phenotype.MicrobiologyOpen · 2024Article
- Limited Adaptation ofMicrobiology spectrum · 2023Article
- The group AInfectious microbes & diseases · 2022Article
- Structure and Function Characterization of the a1a2 Motifs of Streptococcus pyogenes M Protein in Human Plasminogen Binding.Journal of molecular biology · 2019Article
- The Role of Streptococcal and Staphylococcal Exotoxins and Proteases in Human Necrotizing Soft Tissue Infections.Toxins · 2019Review
- A C-terminal CXCL8 peptide based on chemokine-glycosaminoglycan interactions reduces neutrophil adhesion and migration during inflammation.Immunology · 2019Article
- Group AFrontiers in cellular and infection microbiology · 2018Article
- Evolutionary Constraints Shaping Streptococcus pyogenes-Host Interactions.Trends in microbiology · 2017Review
- Article
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Authors and funding
7 authors.
Funding
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Abstract
SpyCEP-mediated chemokine degradation translates into more efficient spreading and increased severity of invasive Group A Streptococcus (GAS) infections, due to impaired neutrophil recruitment to the site of infection. SpyCEP is markedly up-regulated in invasive as compared to colonizing GAS isolates raising the question whether SpyCEP expression hinders bacterial attachment and thus colonization of the host. To address this question we used a molecular approach involving the use of homologous GAS strains either expressing or not SpyCEP or expressing an enzymatically inactive variant of SpyCEP. We found that expression of enzymatically functional SpyCEP lowered GAS adherence and invasion potential toward various epithelial and endothelial cells. SpyCEP also blunted biofilm formation capacity. Our data indicate that expression of SpyCEP decreases colonization and thus might be detrimental for the spreading of GAS.
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Registered trials
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