ArticleInfection and immunity2009
CspA-mediated binding of human factor H inhibits complement deposition and confers serum resistance in Borrelia burgdorferi.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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.
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Who cites it
57 citing papers in PubMed, 79 citations in OpenAlex.
- BBK32 attenuates antibody-dependent complement-mediated killing of infectious Borreliella burgdorferi isolates.PLoS pathogens · 2025Article
- Hitchhiker's Guide toJournal of bacteriology · 2024Review
- Identification of a novel transport system in Borrelia burgdorferi that links the inner and outer membranes.Pathogens and disease · 2023Article
- Microbial evasion of the complement system: a continuous and evolving story.Frontiers in immunology · 2023Review
- Article
- Phylogenomic Diversity Elucidates Mechanistic Insights into Lyme Borreliae-Host Association.mSystems · 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
- A Structural Basis for Inhibition of the Complement Initiator Protease C1r by Lyme Disease Spirochetes.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- The Brilliance ofPathogens (Basel, Switzerland) · 2021Review
- Lyme Disease Pathogenesis.Current issues in molecular biology · 2021Review
- Complement Evasion by Lyme Disease Spirochetes.Trends in microbiology · 2020Review
- New Insights Into CRASP-Mediated Complement Evasion in the Lyme Disease Enzootic Cycle.Frontiers in cellular and infection microbiology · 2020Review
- Complement Evasion inAntibiotics (Basel, Switzerland) · 2019Review
- Outer surface protein polymorphisms linked to host-spirochete association in Lyme borreliae.Molecular microbiology · 2019Review
- Blood treatment of Lyme borreliae demonstrates the mechanism of CspZ-mediated complement evasion to promote systemic infection in vertebrate hosts.Cellular microbiology · 2019Article
- Elucidating the Immune Evasion Mechanisms ofFrontiers in immunology · 2019Article
- A bite so sweet: the glycobiology interface of tick-host-pathogen interactions.Parasites & vectors · 2018Review
- Polymorphic factor H-binding activity of CspA protects Lyme borreliae from the host complement in feeding ticks to facilitate tick-to-host transmission.PLoS pathogens · 2018Article
- Characterization of Stress and Innate Immunity Resistance of Wild-Type and ΔInfection and immunity · 2018Article
- Further Insights Into the Interaction of Human and Animal Complement Regulator Factor H With Viable Lyme Disease Spirochetes.Frontiers in veterinary science · 2018Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Borrelia burgdorferi has developed efficient mechanisms for evading the innate immune response during mammalian infection and has been shown to be resistant to the complement-mediated bactericidal activity of human serum. It is well recognized that B. burgdorferi expresses multiple lipoproteins on its surface that bind the human complement inhibitors factor H and factor H-like protein 1 (FH/FHL-1). The binding of FH/FHL-1 on the surface of B. burgdorferi is thought to enhance its ability to evade serum-mediated killing during the acute phase of infection. One of the key B. burgdorferi FH/FHL-1 binding proteins identified thus far was designated CspA. While it is known that CspA binds FH/FHL-1, it is unclear how the interaction between CspA and FH/FHL-1 specifically enhances serum resistance. To better understand how CspA mediates serum resistance in B. burgdorferi, we inactivated cspA in a virulent strain of B. burgdorferi. An affinity ligand blot immunoassay and indirect immunofluorescence revealed that the CspA mutant does not efficiently bind human FH to its surface. Consistent with the lack of FH binding, the CspA mutant was also highly sensitive to killing by human serum. Additionally, the deposition of complement components C3, C6, and C5b-9 was enhanced on the surface of the CspA mutant compared to that of the wild-type strain. The combined data lead us to conclude that the CspA-mediated binding of human FH confers serum resistance by directly inhibiting complement deposition on the surface of B. burgdorferi.
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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.