ArticleInfection and immunity2007
Borrelia burgdorferi binding of host complement regulator factor H is not required for efficient mammalian infection.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- Mapping the interaction sites of human and avian influenza A viruses and complement factor H.Frontiers in immunology · 2024Article
- Phylogenomic Diversity Elucidates Mechanistic Insights into Lyme Borreliae-Host Association.mSystems · 2022Article
- Utilizing Two Borrelia bavariensis Isolates Naturally Lacking the PFam54 Gene Array To Elucidate the Roles of PFam54-Encoded Proteins.Applied and environmental microbiology · 2022Article
- Host tropism determination by convergent evolution of immunological evasion in the Lyme disease system.PLoS pathogens · 2021Article
- Immune Response toCurrent issues in molecular biology · 2021Article
- Hijacking Factor H for Complement Immune Evasion.Frontiers in immunology · 2021Review
- Lyme Disease Pathogenesis.Current issues in molecular biology · 2021Review
- Complement Evasion by Lyme Disease Spirochetes.Trends in microbiology · 2020Review
- Non-anticoagulant Heparin as a Pre-exposure Prophylaxis Prevents Lyme Disease Infection.ACS infectious diseases · 2020Article
- 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
- 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
- Multifunctional and Redundant Roles ofFrontiers in immunology · 2016Review
- Borrelia burgdorferi BBK32 Inhibits the Classical Pathway by Blocking Activation of the C1 Complement Complex.PLoS pathogens · 2016Article
- ELISA-based measurement of antibody responses and PCR-based detection profiles can distinguish between active infection and early clearance of Borrelia burgdorferi.Clinical & developmental immunology · 2012Article
- Roles for phagocytic cells and complement in controlling relapsing fever infection.Journal of leukocyte biology · 2009Article
- CspA-mediated binding of human factor H inhibits complement deposition and confers serum resistance in Borrelia burgdorferi.Infection and immunity · 2009Article
- Lyme borreliosis spirochete Erp proteins, their known host ligands, and potential roles in mammalian infection.International journal of medical microbiology : IJMM · 2008Review
- Borrelia burgdorferi complement regulator-acquiring surface proteins (BbCRASPs): Expression patterns during the mammal-tick infection cycle.International journal of medical microbiology : IJMM · 2008Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
The causative agent of Lyme disease, Borrelia burgdorferi, is naturally resistant to its host's alternative pathway of complement-mediated killing. Several different borrelial outer surface proteins have been identified as being able to bind host factor H, a regulator of the alternative pathway, leading to a hypothesis that such binding is important for borrelial resistance to complement. To test this hypothesis, the development of B. burgdorferi infection was compared between factor H-deficient and wild-type mice. Factor B- and C3-deficient mice were also studied to determine the relative roles of the alternative and classical/lectin pathways in B. burgdorferi survival during mammalian infection. While it was predicted that B. burgdorferi should be impaired in its ability to infect factor H-deficient animals, quantitative analyses of bacterial loads indicated that those mice were infected at levels similar to those of wild-type and factor B- and C3-deficient mice. Ticks fed on infected factor H-deficient or wild-type mice all acquired similar numbers of bacteria. Indirect immunofluorescence analysis of B. burgdorferi acquired by feeding ticks from the blood of infected mice indicated that none of the bacteria had detectable levels of factor H on their outer surfaces, even though such bacteria express high levels of surface proteins capable of binding factor H. These findings demonstrate that the acquisition of host factor H is not essential for mammalian infection by B. burgdorferi and indicate that additional mechanisms are employed by the Lyme disease spirochete to evade complement-mediated killing.
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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.