ArticleInfection and immunity2006
Fibronectin binding protein BBK32 of the Lyme disease spirochete promotes bacterial attachment to glycosaminoglycans.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
105 citing papers in PubMed, 157 citations in OpenAlex.
- Innate immune responses tomBio · 2026Article
- The BosR Is Back!Molecular microbiology · 2026Article
- The wild, wild west of plasmids: First insights into comparative genomics of Borrelia burgdorferi sensu lato.PloS one · 2026Article
- The diagnostic potential of proteomics and machine learning in Lyme neuroborreliosis.Nature communications · 2025Article
- Navigating infection by pathogenic spirochetes: The host-bacteria interface at the atomic level.Protein science : a publication of the Protein Society · 2025Review
- Borrelia surface proteins: new horizons in Lyme disease diagnosis.Applied microbiology and biotechnology · 2025Review
- Heterologous Surface Display Reveals Conserved Complement Inhibition and Functional Diversification of Borrelia burgdorferi Elp Proteins.Molecular microbiology · 2025Article
- BBK32 attenuates antibody-dependent complement-mediated killing of infectious Borreliella burgdorferi isolates.PLoS pathogens · 2025Article
- Revisiting Host-Binding Properties of LigA and LigB Recombinant Domains.Microorganisms · 2025Article
- AncientScience (New York, N.Y.) · 2025Article
- Extravasation of Borrelia burgdorferi Across the Blood-Brain Barrier is an Extremely Rare Event.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Secreted Metabolites fromMicroorganisms · 2024Article
- Pathogenicity and virulence ofVirulence · 2023Review
- Review
- Carbohydrates: Binding Sites and Potential Drug Targets for Neural-Affecting Pathogens.Advances in neurobiology · 2023Article
- Transmission Cycle of Tick-Borne Infections and Co-Infections, Animal Models and Diseases.Pathogens (Basel, Switzerland) · 2022Review
- 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
- Potential Regulatory Role in Mammalian Host Adaptation for a Small Intergenic Region of Lp17 in the Lyme Disease Spirochete.Frontiers in cellular and infection microbiology · 2022Article
- A Structural Basis for Inhibition of the Complement Initiator Protease C1r by Lyme Disease Spirochetes.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Borrelia burgdorferi, the agent of Lyme disease, causes a multisystemic illness that can affect the skin, heart, joints, and nervous system and is capable of attachment to diverse cell types. Among the host components recognized by this spirochete are fibronectin and glycosaminoglycans (GAGs). Three surface-localized GAG-binding bacterial ligands, Bgp, DbpA, and DbpB, have been previously identified, but recent studies suggested that at least one additional GAG-binding ligand is expressed on the spirochetal surface when the spirochete is adapted to the mammalian host environment. BBK32 is a surface lipoprotein that is produced during infection and that has been shown to bind to fibronectin. In this study, we show that, when BBK32 was produced from a shuttle vector in an otherwise nonadherent high-passage B. burgdorferi strain, the protein localized on the bacterial surface and conferred attachment to fibronectin and to mammalian cell monolayers. In addition, the high-passage strain producing BBK32 bound to purified preparations of the GAGs dermatan sulfate and heparin, as well as to these GAGs on the surfaces of cultured mammalian cells. Recombinant BBK32 recognized purified heparin, indicating that the bacterial attachment to GAGs was due to direct binding by BBK32. This GAG-binding activity of BBK32 is apparently independent of fibronectin recognition, because exogenous heparin had no effect on BBK32-mediated bacterial binding to fibronectin.
Indexed as
Identifiers
What OpenQuestion holds
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.