ArticleInfection and immunity2009
Analysis of a unique interaction between the complement regulatory protein factor H and the periodontal pathogen Treponema denticola.
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 43 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.
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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
43 citing papers in PubMed, 63 citations in OpenAlex.
- Expanded Functional Characterization and Optimization of Protein Expression in Treponema denticola Shuttle Plasmids.Molecular oral microbiology · 2026Article
- Navigating infection by pathogenic spirochetes: The host-bacteria interface at the atomic level.Protein science : a publication of the Protein Society · 2025Review
- Periodontal and microbiological data in patients with mucous membrane pemphigoid in a French population in 2021-2022: A pilot cross-sectional study.Health science reports · 2024Article
- The Leptospiral General Secretory Protein D (GspD), a secretin, elicits complement-independent bactericidal antibody against diverseVaccine: X · 2021Article
- Human and Veterinary Vaccines for Lyme Disease.Current issues in molecular biology · 2021Article
- Hijacking Factor H for Complement Immune Evasion.Frontiers in immunology · 2021Review
- Roles of TroA and TroR in Metalloregulated Growth and Gene Expression inJournal of bacteriology · 2020Article
- Article
- Ehrlichia chaffeensis EplA Interaction With Host Cell Protein Disulfide Isomerase Promotes Infection.Frontiers in cellular and infection microbiology · 2020Article
- Salivary Total Protease Activity Based on a Broad-Spectrum Fluorescence Resonance Energy Transfer Approach to Monitor Induction and Resolution of Gingival Inflammation.Molecular diagnosis & therapy · 2019Article
- Treponema denticola increases MMP-2 expression and activation in the periodontium via reversible DNA and histone modifications.Cellular microbiology · 2018Article
- Factor H Family Proteins in Complement Evasion of Microorganisms.Frontiers in immunology · 2017Review
- FACIN, a Double-Edged Sword of the Emerging Periodontal Pathogen Filifactor alocis: A Metabolic Enzyme Moonlighting as a Complement Inhibitor.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- The Treponema denticola FhbB Protein Is a Dominant Early Antigen That Elicits FhbB Variant-Specific Antibodies That Block Factor H Binding and Cleavage by Dentilisin.Infection and immunity · 2016Article
- Polymicrobial synergy and dysbiosis in inflammatory disease.Trends in molecular medicine · 2015Review
- Complement Involvement in Periodontitis: Molecular Mechanisms and Rational Therapeutic Approaches.Advances in experimental medicine and biology · 2015Review
- The outer membrane protease PgtE of Salmonella enterica interferes with the alternative complement pathway by cleaving factors B and H.Frontiers in microbiology · 2015Article
- Analysis of the complement sensitivity of oral treponemes and the potential influence of FH binding, FH cleavage and dentilisin activity on the pathogenesis of periodontal disease.Molecular oral microbiology · 2014Article
- The Borrelia hermsii factor H binding protein FhbA is not required for infectivity in mice or for resistance to human complement in vitro.Infection and immunity · 2014Article
- Genetic and intervention studies implicating complement C3 as a major target for the treatment of periodontitis.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Treponema denticola, a spirochete associated with periodontitis, is abundant at the leading edge of subgingival plaque, where it interacts with gingival epithelia. T. denticola produces a number of virulence factors, including dentilisin, a protease which is cytopathic to host cells, and FhbB, a unique T. denticola lipoprotein that binds complement regulatory proteins. Earlier analyses suggested that FhbB specifically bound to factor H (FH)-like protein 1 (FHL-1). However, by using dentilisin-deficient mutants of T. denticola, we found that T. denticola preferentially binds FH and not FHL-1, and that FH is then cleaved by dentilisin to yield an FH subfragment of approximately 50 kDa. FH bound to dentilisin-deficient mutants but was not cleaved and retained its ability to serve as a cofactor for factor I in the cleavage of C3b. To assess the molecular basis of the interaction of FhbB with FH, mutational analyses were conducted. Replacement of specific residues in widely separated domains of FhbB and disruption of a central alpha helix with coiled-coil formation probability attenuated or eliminated FH binding. The data presented here are the first to demonstrate the retention at the cell surface of a proteolytic cleavage product of FH. The precise role of this FH fragment in the host-pathogen interaction remains to be determined.
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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.