ArticleJournal of innate immunity2014
Plasmin(ogen) acquisition by group A Streptococcus protects against C3b-mediated neutrophil killing.
Article in Journal of innate immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Clinical and Epidemiological Landscape of Antimicrobial Resistance and Virulence inAntibiotics (Basel, Switzerland) · 2026Review
- Group A Streptococcal Virulence Factors and Vaccine Development-An Update.Microorganisms · 2026Review
- Proteins of the SubB family provide multiple mechanisms of serum resistance inEmerging microbes & infections · 2025Article
- Review
- Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024Review
- Contribution of Streptococcus pyogenes M87 protein to innate immune resistance and virulence.Microbial pathogenesis · 2022Article
- Interaction of helminth parasites with the haemostatic system of their vertebrate hosts: a scoping review.Parasite (Paris, France) · 2022Article
- Nonimmune antibody interactions of Group A Streptococcus M and M-like proteins.PLoS pathogens · 2021Review
- Inflammatory Protein Profiles in Plasma of Candidaemia Patients and the Contribution of Host Genetics to Their Variability.Frontiers in immunology · 2021Article
- Article
- Catch Me if You Can: Streptococcus pyogenes Complement Evasion Strategies.Journal of innate immunity · 2019Review
- Toxins and Superantigens of Group A Streptococci.Microbiology spectrum · 2019Article
- Human IgG Increases Virulence ofJournal of immunology (Baltimore, Md. : 1950) · 2018Article
- Innate Immune Interactions betweenFrontiers in cellular and infection microbiology · 2018Article
- Factor H-IgG Chimeric Proteins as a Therapeutic Approach against the Gram-Positive Bacterial PathogenJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- Blood Group Antigen Recognition via the Group A Streptococcal M Protein Mediates Host Colonization.mBio · 2017Article
- Bacterial Evasion of Host Antimicrobial Peptide Defenses.Microbiology spectrum · 2016Review
- Streptococcus pyogenes Escapes Killing from Extracellular Histones through Plasminogen Binding and Activation by Streptokinase.Journal of innate immunity · 2016Article
- Group A Streptococcus Modulates Host Inflammation by Manipulating Polymorphonuclear Leukocyte Cell Death Responses.Journal of innate immunity · 2015Article
- Disease manifestations and pathogenic mechanisms of Group A Streptococcus.Clinical microbiology reviews · 2014Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
The globally significant human pathogen group A Streptococcus (GAS) sequesters the host protease plasmin to the cell surface during invasive disease initiation. Recent evidence has shown that localized plasmin activity prevents opsonization of several bacterial species by key components of the innate immune system in vitro. Here we demonstrate that plasmin at the GAS cell surface resulted in degradation of complement factor C3b, and that plasminogen acquisition is associated with a decrease in C3b opsonization and neutrophil-mediated killing in vitro. Furthermore, the ability to acquire cell surface plasmin(ogen) correlates directly with a decrease in C3b opsonization, neutrophil phagocytosis, and increased bacterial survival in a humanized plasminogen mouse model of infection. These findings demonstrate that localized plasmin(ogen) plays an important role in facilitating GAS escape from the host innate immune response and increases bacterial virulence in the early stages of infection.
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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.