ArticleInfection and immunity2010
Human platelets recognize a novel surface protein, PadA, on Streptococcus gordonii through a unique interaction involving fibrinogen receptor GPIIbIIIa.
Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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Who cites it
36 citing papers in PubMed, 76 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
- Loss of Fsr quorum sensing promotes biofilm formation and worsens outcomes in enterococcal infective endocarditis.Nature communications · 2026Article
- Platelets in infection: intrinsic roles and functional outcomes.Frontiers in immunology · 2025Review
- Bacterial interactions with platelets: defining key themes.Frontiers in immunology · 2025Review
- Identification ofmBio · 2024Article
- Article
- Blood Platelets in Infection: The Multiple Roles of the Platelet Signalling Machinery.International journal of molecular sciences · 2023Review
- Role of Platelets in Detection and Regulation of Infection.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Uncovering Roles of Streptococcus gordonii SrtA-Processed Proteins in the Biofilm Lifestyle.Journal of bacteriology · 2020Article
- Platelet plug formation in whole blood is enhanced in the presence of Porphyromonas gingivalis.Molecular oral microbiology · 2020Article
- Review
- From Classical to Unconventional: The Immune Receptors Facilitating Platelet Responses to Infection and Inflammation.Biology · 2020Review
- Drug TargetingSmall structures · 2020Article
- A Champion of Host Defense: A Generic Large-Scale Cause for Platelet Dysfunction and Depletion in Infection.Seminars in thrombosis and hemostasis · 2020Review
- Platelets Are Critical Key Players in Sepsis.International journal of molecular sciences · 2019Review
- Recognition of specific sialoglycan structures by oral streptococci impacts the severity of endocardial infection.PLoS pathogens · 2019Article
- Genetics ofMicrobiology spectrum · 2019Article
- Early Host Interactions That Drive the Dysregulated Response in Sepsis.Frontiers in immunology · 2019Review
- Role of Neuraminidase-Producing Bacteria in Exposing Cryptic Carbohydrate Receptors for Streptococcus gordonii Adherence.Infection and immunity · 2018Article
- Macrophage Polarization Alters Postphagocytosis Survivability of the Commensal Streptococcus gordonii.Infection and immunity · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
The concept of an infectious agent playing a role in cardiovascular disease is slowly gaining attention. Among several pathogens identified, the oral bacterium Streptococcus gordonii has been implicated as a plausible agent. Platelet adhesion and subsequent aggregation are critical events in the pathogenesis and dissemination of the infective process. Here we describe the identification and characterization of a novel cell wall-anchored surface protein, PadA (397 kDa), of S. gordonii DL1 that binds to the platelet fibrinogen receptor GPIIbIIIa. Wild-type S. gordonii cells induced platelet aggregation and supported platelet adhesion in a GPIIbIIIa-dependent manner. Deletion of the padA gene had no effect on platelet aggregation by S. gordonii but significantly reduced (>75%) platelet adhesion to S. gordonii. Purified N-terminal PadA recombinant polypeptide adhered to platelets. The padA mutant was unaffected in production of other platelet-interactive surface proteins (Hsa, SspA, and SspB), and levels of adherence of the mutant to fetuin or platelet receptor GPIb were unaffected. Wild-type S. gordonii, but not the padA mutant, bound to Chinese hamster ovary cells stably transfected with GPIIbIIIa, and this interaction was ablated by addition of GPIIbIIIa inhibitor Abciximab. These results highlight the growing complexity of interactions between S. gordonii and platelets and demonstrate a new mechanism by which the bacterium could contribute to unwanted thrombosis.
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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.