ArticlePloS one2013
Role of the serine-rich surface glycoprotein Srr1 of Streptococcus agalactiae in the pathogenesis of infective endocarditis.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 47 citations in OpenAlex.
- Oral streptococci utilize a Siglec-like domain of serine-rich repeat adhesins to preferentially target platelet sialoglycans in human blood.PLoS pathogens · 2014Trial
- Emergence, identification, and characterization of a novel Streptococcus agalactiae CPS type Ia ST7 strain (Ia-2021) causing large scale mortalities in tilapia aquaculture.Scientific reports · 2026Article
- Biofilms and oral health: nanotechnology for biofilm control.Discover nano · 2025Review
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- Analysis of serotype distribution and characteristics of nonhemolytic and nonpigmented strains among group B Streptococcus isolates in a southern Taiwan local hospital.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025Article
- Re-framing the importance of Group BInfection and immunity · 2024Review
- Serine-rich repeat proteins: well-known yet little-understood bacterial adhesins.Journal of bacteriology · 2024Review
- The Role of Platelets in Infective Endocarditis.International journal of molecular sciences · 2023Review
- Streptococcus agalactiae infective endocarditis in Canada: a multicenter retrospective nested case control analysis.BMC infectious diseases · 2022Article
- Article
- Article
- A novel sialic acid-binding adhesin present in multiple species contributes to the pathogenesis of Infective endocarditis.PLoS pathogens · 2021Article
- Tandem sialoglycan-binding modules in aThe Journal of biological chemistry · 2020Article
- Genome-Wide Assessment of Streptococcus agalactiae Genes Required for Survival in Human Whole Blood and Plasma.Infection and immunity · 2020Article
- Beta-Hemolytic Streptococcal Infective Endocarditis: Characteristics and Outcomes From a Large, Multinational Cohort.Open forum infectious diseases · 2020Article
- Serine-rich repeat proteins from gut microbes.Gut microbes · 2020Review
- Streptococcal Serine-Rich Repeat Proteins in Colonization and Disease.Frontiers in microbiology · 2020Review
- Streptococcus oralis subsp.Infection and immunity · 2019Article
- Recognition of specific sialoglycan structures by oral streptococci impacts the severity of endocardial infection.PLoS pathogens · 2019Article
- The Two Distinct Types of SecA2-Dependent Export Systems.Microbiology spectrum · 2019Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The binding of bacteria to fibrinogen and platelets are important events in the pathogenesis of infective endocarditis. Srr1 is a serine-rich repeat glycoprotein of Streptococcus agalactiae that binds directly to the Aα chain of human fibrinogen. To assess the impact of Srr1 on the pathogenesis of endocarditis due to S. agalactiae, we first examined the binding of this organism to immobilized human platelets. Strains expressing Srr1 had significantly higher levels of binding to human platelets in vitro, as compared with isogenic Δsrr1 mutants. In addition, platelet binding was inhibited by pretreatment with anti-fibrinogen IgG or purified Srr1 binding region. To assess the contribution of Srr1 to pathogenicity, we compared the relative virulence of S. agalactiae NCTC 10/84 strain and its Δsrr1 mutant in a rat model of endocarditis, where animals were co-infected with the WT and the mutant strains at a 1:1 ratio. At 72 h post-infection, bacterial densities (CFU/g) of the WT strain within vegetations, kidneys, and spleens were significantly higher, as compared with the Δsrr1 mutant. These results indicate that Srr1 contributes to the pathogenesis of endocarditis due to S. agalactiae, at least in part through its role in fibrinogen-mediated platelet binding.
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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.