ArticleCellular microbiology2015
Glycosaminoglycan binding by Borrelia burgdorferi adhesin BBK32 specifically and uniquely promotes joint colonization.
Article in Cellular microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 72 citations in OpenAlex.
- Machine learning-driven identification of virulence determinants in Borrelia burgdorferi associated with human dissemination.PLoS computational biology · 2026Article
- In vitro and in vivo endothelial interactions of Leptospira species are markers of virulence.PLoS neglected tropical diseases · 2026Article
- BBK32 attenuates antibody-dependent complement-mediated killing of infectious Borreliella burgdorferi isolates.PLoS pathogens · 2025Article
- Borrelia surface proteins: new horizons in Lyme disease diagnosis.Applied microbiology and biotechnology · 2025Review
- Extravasation of Borrelia burgdorferi Across the Blood-Brain Barrier is an Extremely Rare Event.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Leucine-rich repeat proteins ofFrontiers in microbiology · 2024Article
- Pathogenicity and virulence ofVirulence · 2023Review
- VlsE, the nexus for antigenic variation of the Lyme disease spirochete, also mediates early bacterial attachment to the host microvasculature under shear force.PLoS pathogens · 2022Article
- Lipoproteome screening of the Lyme disease agent identifies inhibitors of antibody-mediated complement killing.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The evolving story of Borrelia burgdorferi sensu lato transmission in Europe.Parasitology research · 2022Review
- Identification of amino acid domains ofFrontiers in cellular and infection microbiology · 2022Article
- Article
- The leptospiral LipL21 and LipL41 proteins exhibit a broad spectrum of interactions with host cell components.Virulence · 2021Article
- Article
- Lyme Disease Pathogenesis.Current issues in molecular biology · 2021Review
- Lyme Disease in Humans.Current issues in molecular biology · 2021Article
- Complement Evasion by Lyme Disease Spirochetes.Trends in microbiology · 2020Review
- BBB07 contributes to, but is not essential for,Microbiology (Reading, England) · 2020Article
- Complement Evasion Contributes to Lyme Borreliae-Host Associations.Trends in parasitology · 2020Review
- Strain-specific joint invasion and colonization by Lyme disease spirochetes is promoted by outer surface protein C.PLoS pathogens · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Microbial pathogens that colonize multiple tissues commonly produce adhesive surface proteins that mediate attachment to cells and/or extracellular matrix in target organs. Many of these 'adhesins' bind to multiple ligands, complicating efforts to understand the role of each ligand-binding activity. Borrelia burgdorferi, the causative agent of Lyme disease, produces BBK32, first identified as a fibronectin-binding adhesin that promotes skin and joint colonization. BBK32 also binds to glycosaminoglycan (GAG), which, like fibronectin is ubiquitously present on cell surfaces. To determine which binding activity is relevant for BBK32-promoted infectivity, we generated a panel of BBK32 truncation and internal deletion mutants, and identified variants specifically defective for binding to either fibronectin or GAG. These variants promoted bacterial attachment to different mammalian cell types in vitro, suggesting that fibronectin and GAG binding may play distinct roles during infection. Intravenous inoculation of mice with a high-passage non-infectious B. burgdorferi strain that produced wild-type BBK32 or BBK32 mutants defective for GAG or fibronectin binding, revealed that only GAG-binding activity was required for significant localization to joints at 60 min post-infection. An otherwise infectious B. burgdorferi strain producing BBK32 specifically deficient in fibronectin binding was fully capable of both skin and joint colonization in the murine model, whereas a strain producing BBK32 selectively attenuated for GAG binding colonized the inoculation site but not knee or tibiotarsus joints. Thus, the BBK32 fibronectin- and GAG-binding activities are separable in vivo, and BBK32-mediated GAG binding, but not fibronectin binding, contributes to joint colonization.
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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.