ArticleInfection and immunity2013
The early dissemination defect attributed to disruption of decorin-binding proteins is abolished in chronic murine Lyme borreliosis.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
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
28 citing papers in PubMed, 38 citations in OpenAlex.
- Machine learning-driven identification of virulence determinants in Borrelia burgdorferi associated with human dissemination.PLoS computational biology · 2026Article
- Multiplexed single-tier immunoassay for improved Lyme disease diagnosis across all disease stages.Research square · 2026Article
- Characterizing the impact of intracutaneous dissemination on host responses duringFrontiers in immunology · 2026Article
- Evaluation of Immune Response Dynamics: Analyzing the Parameters of Complete Blood Count (CBC) in Experimental Borreliosis.Life (Basel, Switzerland) · 2025Article
- Targeted volume imaging reveals early vascular interactions of Lyme disease pathogen in skin.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
- Pathogenicity and virulence ofVirulence · 2023Review
- Choreography of Lyme Disease Spirochete Adhesins To Promote Vascular Escape.Microbiology spectrum · 2023Article
- Nanomechanical mechanisms of Lyme disease spirochete motility enhancement in extracellular matrix.Communications biology · 2021Article
- Lyme Disease Pathogenesis.Current issues in molecular biology · 2021Review
- Immune Response toCurrent issues in molecular biology · 2021Article
- The BB0345 Hypothetical Protein of Borrelia burgdorferi Is Essential for Mammalian Infection.Infection and immunity · 2020Article
- Serologic Evidence for the Exposure of Eastern Coyotes (mSphere · 2020Article
- Borrelia burgdorferi spatiotemporal regulation of transcriptional regulator bosR and decorin binding protein during murine infection.Scientific reports · 2020Article
- A bite so sweet: the glycobiology interface of tick-host-pathogen interactions.Parasites & vectors · 2018Review
- Review
- Review
- Middle region of the Borrelia burgdorferi surface-located protein 1 (Lmp1) interacts with host chondroitin-6-sulfate and independently facilitates infection.Cellular microbiology · 2016Article
- Structure of decorin binding protein B from Borrelia burgdorferi and its interactions with glycosaminoglycans.Biochimica et biophysica acta · 2015Article
- Borrelia burgdorferi RevA Significantly Affects Pathogenicity and Host Response in the Mouse Model of Lyme Disease.Infection and immunity · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The laboratory mouse model of Lyme disease has revealed that Borrelia burgdorferi differentially expresses numerous outer surface proteins that influence different stages of infection (tick-borne transmission, tissue colonization, dissemination, persistence, and tick acquisition). Deletion of two such outer surface proteins, decorin-binding proteins A and B (DbpA/B), has been documented to decrease infectivity, impede early dissemination, and, possibly, prevent persistence. In this study, DbpA/B-deficient spirochetes were confirmed to exhibit an early dissemination defect in immunocompetent, but not immunodeficient, mice, and the defect was found to resolve with chronicity. Development of disease (arthritis and carditis) was attenuated only in the early stage of infection with DbpA/B-deficient spirochetes in both types of mice. Persistence of the DbpA/B-deficient spirochetes occurred in both immunocompetent and immunodeficient mice in a manner indistinguishable from that of wild-type spirochetes. Dissemination through the lymphatic system was evaluated as an underlying mechanism for the early dissemination defect. At 12 h, 3 days, 7 days, and 14 days postinoculation, DbpA/B-deficient spirochetes were significantly less prevalent and in lower numbers in lymph nodes than wild-type spirochetes. However, in immunodeficient mice, deficiency of DbpA/B did not significantly decrease the prevalence or spirochete numbers in lymph nodes. Complementation of DbpA/B restored a wild-type phenotype. Thus, the results indicated that deficiency of DbpA/B allows the acquired immune response to restrict early dissemination of spirochetes, which appears to be at least partially mediated through the lymphatic system.
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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.