ArticlePLoS pathogens2017
Multi-functional mechanisms of immune evasion by the streptococcal complement inhibitor C5a peptidase.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 84 citations in OpenAlex.
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- Group A Streptococcal Virulence Factors and Vaccine Development-An Update.Microorganisms · 2026Review
- The roles of theJournal of bacteriology · 2026Article
- Proteins of the SubB family provide multiple mechanisms of serum resistance inEmerging microbes & infections · 2025Article
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Global spread of Streptococcus pyogenes A genomics-supported narrative review.FEMS microbiology reviews · 2025Review
- Advances in Necrotizing Fasciitis Animal Models: Current Trends and Future Perspectives.Journal of inflammation research · 2025Review
- The intricate pathogenicity of Group AVirulence · 2024Review
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- The complement system: A key player in the host response to infections.European journal of immunology · 2024Review
- A novel infective endocarditis virulence factor related to multiple functions for bacterial survival in blood was discovered inbioRxiv : the preprint server for biology · 2024Article
- Determinants of bacterial survival and proliferation in blood.FEMS microbiology reviews · 2024Review
- Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024Review
- Comparative analysis of the interactions of different Streptococcus suis strains with monocytes, granulocytes and the complement system in porcine blood.Veterinary research · 2024Article
- Secretome analysis and virulence assessment inJournal of oral microbiology · 2024Article
- Metatranscriptomic analysis shows functional alterations in subgingival biofilm in young smokers with periodontitis: a pilot study.Journal of applied oral science : revista FOB · 2024Observational
- PepO and CppA modulateVirulence · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The complement cascade is crucial for clearance and control of invading pathogens, and as such is a key target for pathogen mediated host modulation. C3 is the central molecule of the complement cascade, and plays a vital role in opsonization of bacteria and recruitment of neutrophils to the site of infection. Streptococcal species have evolved multiple mechanisms to disrupt complement-mediated innate immunity, among which ScpA (C5a peptidase), a C5a inactivating enzyme, is widely conserved. Here we demonstrate for the first time that pyogenic streptococcal species are capable of cleaving C3, and identify C3 and C3a as novel substrates for the streptococcal ScpA, which are functionally inactivated as a result of cleavage 7 amino acids upstream of the natural C3 convertase. Cleavage of C3a by ScpA resulted in disruption of human neutrophil activation, phagocytosis and chemotaxis, while cleavage of C3 generated abnormally-sized C3a and C3b moieties with impaired function, in particular reducing C3 deposition on the bacterial surface. Despite clear effects on human complement, expression of ScpA reduced clearance of group A streptococci in vivo in wildtype and C5 deficient mice, and promoted systemic bacterial dissemination in mice that lacked both C3 and C5, suggesting an additional complement-independent role for ScpA in streptococcal pathogenesis. ScpA was shown to mediate streptococcal adhesion to both human epithelial and endothelial cells, consistent with a role in promoting bacterial invasion within the host. Taken together, these data show that ScpA is a multi-functional virulence factor with both complement-dependent and independent roles in streptococcal pathogenesis.
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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.