ArticleThe EMBO journal2006
A streptococcal protease that degrades CXC chemokines and impairs bacterial clearance from infected tissues.
Article in The EMBO journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
65 citing papers in PubMed, 156 citations in OpenAlex.
- Group A Streptococcus secreted esterase hydrolyzes platelet-activating factor to impede neutrophil recruitment and facilitate innate immune evasion.PLoS pathogens · 2012Trial
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- Neutrophil diversity and function in health and disease.Signal transduction and targeted therapy · 2024Review
- EmergentInfection and immunity · 2024Article
- Immunomodulating Enzymes fromMicroorganisms · 2024Review
- Streptococcal peptides and their roles in host-microbe interactions.Frontiers in cellular and infection microbiology · 2023Review
- The group AInfectious microbes & diseases · 2022Article
- The Role of Streptococcal Cell-Envelope Proteases in Bacterial Evasion of the Innate Immune System.Journal of innate immunity · 2022Review
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- Group A Streptococcus Infection of the Nasopharynx Requires Proinflammatory Signaling through the Interleukin-1 Receptor.Infection and immunity · 2020Article
- Alternative approaches to treat bacterial infections: targeting quorum-sensing.Expert review of anti-infective therapy · 2020Review
- The Versatility of Opportunistic Infections Caused byFrontiers in microbiology · 2020Article
- The Role of Streptococcal and Staphylococcal Exotoxins and Proteases in Human Necrotizing Soft Tissue Infections.Toxins · 2019Review
- A Requirement for Neutrophil Glycosaminoglycans in Chemokine:Receptor Interactions Is Revealed by the Streptococcal Protease SpyCEP.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Lipoteichoic acid anchor triggers Mincle to drive protective immunity against invasive group AProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Neutrophils and Bacterial Immune Evasion.Journal of innate immunity · 2018Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group A Streptococcus (GAS) causes the life-threatening infection in humans known as necrotizing fasciitis (NF). Infected subcutaneous tissues from an NF patient and mice challenged with the same GAS strain possessed high bacterial loads but a striking paucity of infiltrating polymorphonuclear leukocytes (PMNs). Impaired PMN recruitment was attributed to degradation of the chemokine IL-8 by a GAS serine peptidase. Here, we use bioinformatics approach coupled with target mutagenesis to identify this peptidase as ScpC. We show that SilCR pheromone downregulates scpC transcription via the two-component system-SilA/B. In addition, we demonstrate that in vitro, ScpC degrades the CXC chemokines: IL-8 (human), KC, and MIP-2 (both murine). Furthermore, using a murine model of human NF, we demonstrate that ScpC, but not the C5a peptidase ScpA, is an essential virulence factor. An ScpC-deficient mutant is innocuous for untreated mice but lethal for PMN-depleted mice. ScpC degrades KC and MIP-2 locally in the infected skin tissues, inhibiting PMN recruitment. In conclusion, ScpC represents a novel GAS virulence factor functioning to directly inactivate a key element of the host innate immune response.
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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.