ArticleProceedings of the National Academy of Sciences of the United States of America2002
Insight into the molecular basis of pathogen abundance: group A Streptococcus inhibitor of complement inhibits bacterial adherence and internalization into human cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 88 citations in OpenAlex.
- Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024Review
- Mechanisms that potentially contribute to the development of post-streptococcal glomerulonephritis.Pathogens and disease · 2024Review
- BifA Triggers Phosphorylation of Ezrin to BenefitBiomedicines · 2022Article
- Understanding nanoparticle endocytosis to improve targeting strategies in nanomedicine.Chemical Society reviews · 2021Review
- Article
- Vaccine-induced, but not natural immunity, against the Streptococcal inhibitor of complement protects against invasive disease.NPJ vaccines · 2021Article
- Group AMicrobiology spectrum · 2019Article
- Streptococcal inhibitor of complement (SIC) modulates fibrinolysis and enhances bacterial survival within fibrin clots.The Journal of biological chemistry · 2018Article
- Paediatric Autoimmune Neuropsychiatric Disorder Associated with Group A Beta-Haemolytic Streptococcal Infection: An Indication for Tonsillectomy? A Review of the Literature.International journal of otolaryngology · 2018Review
- Mechanisms of group A Streptococcus resistance to reactive oxygen species.FEMS microbiology reviews · 2015Review
- Disease manifestations and pathogenic mechanisms of Group A Streptococcus.Clinical microbiology reviews · 2014Review
- Responses of innate immune cells to group A Streptococcus.Frontiers in cellular and infection microbiology · 2014Review
- Interaction between M-like protein and macrophage thioredoxin facilitates antiphagocytosis for Streptococcus equi ssp. zooepidemicus.PloS one · 2012Article
- Streptococcus pyogenes Ser/Thr kinase-regulated cell wall hydrolase is a cell division plane-recognizing and chain-forming virulence factor.The Journal of biological chemistry · 2010Article
- Streptococcal inhibitor of complement promotes innate immune resistance phenotypes of invasive M1T1 group A Streptococcus.Journal of innate immunity · 2010Article
- Inactivation of DltA modulates virulence factor expression in Streptococcus pyogenes.PloS one · 2009Article
- Species-specific interaction of Streptococcus pneumoniae with human complement factor H.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Dynamics in prophage content of invasive and noninvasive M1 and M28 Streptococcus pyogenes isolates in The Netherlands from 1959 to 1996.Infection and immunity · 2007Article
- Determination of the relationship between group A streptococcal genome content, M type, and toxic shock syndrome by a mixed genome microarray.Infection and immunity · 2007Article
- Dynamics of the immune response against extracellular products of group A streptococci during infection.Clinical and vaccine immunology : CVI · 2007Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Streptococcal inhibitor of complement (Sic) is a secreted protein made predominantly by serotype M1 Group A Streptococcus (GAS), which contributes to persistence in the mammalian upper respiratory tract and epidemics of human disease. Unexpectedly, an isogenic sic-negative mutant adhered to human epithelial cells significantly better than the wild-type parental strain. Purified Sic inhibited the adherence of a sic negative serotype M1 mutant and of non-Sic-producing GAS strains to human epithelial cells. Sic was rapidly internalized by human epithelial cells, inducing cell flattening and loss of microvilli. Ezrin and moesin, human proteins that functionally link the cytoskeleton to the plasma membrane, were identified as Sic-binding proteins by affinity chromatography and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry analysis. Sic colocalized with ezrin inside epithelial cells and bound to the F-actin-binding site region located in the carboxyl terminus of ezrin and moesin. Synthetic peptides corresponding to two regions of Sic had GAS adherence-inhibitory activity equivalent to mature Sic and inhibited binding of Sic to ezrin. In addition, the sic mutant was phagocytosed and killed by human polymorphonuclear leukocytes significantly better than the wild-type strain, and Sic colocalized with ezrin in discrete regions of polymorphonuclear leukocytes. The data suggest that binding of Sic to ezrin alters cellular processes critical for efficient GAS contact, internalization, and killing. Sic enhances bacterial survival by enabling the pathogen to avoid the intracellular environment. This process contributes to the abundance of M1 GAS in human infections and their ability to cause epidemics.
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