ArticleMolecular oral microbiology2011
Identification of the primary mechanism of complement evasion by the periodontal pathogen, Treponema denticola.
Article in Molecular oral microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 51 citations in OpenAlex.
- Expanded Functional Characterization and Optimization of Protein Expression in Treponema denticola Shuttle Plasmids.Molecular oral microbiology · 2026Article
- Nisin bacteriocin blocks T. denticola-triggered MMP2 activation and pathogen internalization via TLR2.Scientific reports · 2026Article
- Revisiting Host-Binding Properties of LigA and LigB Recombinant Domains.Microorganisms · 2025Article
- A bipartite bacterial virulence factor targets the complement system and neutrophil activation.The EMBO journal · 2025Article
- Molecular Analysis ofPathogens (Basel, Switzerland) · 2024Article
- Purification of Native Dentilisin Complex fromBio-protocol · 2024Article
- Recent Aspects of Periodontitis and Alzheimer's Disease-A Narrative Review.International journal of molecular sciences · 2024Review
- Enhanced transformation efficiency in Treponema denticola enabled by SyngenicDNA-based plasmids lacking restriction-modification target motifs.Molecular oral microbiology · 2023Article
- Subversion of the immune response of human pathogenic spirochetes.Journal of clinical laboratory analysis · 2022Review
- Approaches to Understanding Mechanisms of Dentilisin Protease Complex Expression inFrontiers in cellular and infection microbiology · 2021Review
- Periodontal pathogens promote cancer aggressivity via TLR/MyD88 triggered activation of Integrin/FAK signaling that is therapeutically reversible by a probiotic bacteriocin.PLoS pathogens · 2020Article
- Blood treatment of Lyme borreliae demonstrates the mechanism of CspZ-mediated complement evasion to promote systemic infection in vertebrate hosts.Cellular microbiology · 2019Article
- Treponema denticola increases MMP-2 expression and activation in the periodontium via reversible DNA and histone modifications.Cellular microbiology · 2018Article
- The major outer sheath protein forms distinct conformers and multimeric complexes in the outer membrane and periplasm of Treponema denticola.Scientific reports · 2017Article
- 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
- Porphyromonas gingivalis Periodontal Infection and Its Putative Links with Alzheimer's Disease.Mediators of inflammation · 2015Review
- The Treponema denticola AtcR LytTR domain-containing response regulator interacts with three architecturally distinct promoter elements: implications for understanding the molecular signaling mechanisms that drive the progression of periodontal disease.Molecular oral microbiology · 2014Article
- 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 Cross-Talk between Spirochetal Lipoproteins and Immunity.Frontiers in immunology · 2014Review
- A surface-exposed neuraminidase affects complement resistance and virulence of the oral spirochaete Treponema denticola.Molecular microbiology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Treponema denticola, a periodontal pathogen, binds the complement regulatory protein Factor H (FH). Factor H binding protein B (FhbB) is the sole FH binding protein produced by T. denticola. The interaction of FhbB with FH is unique in that FH is bound to the cell and then cleaved by the T. denticola protease, dentilisin. A ∼ 50-kDa product generated by dentilisin cleavage is retained at the cell surface. Until this study, a direct role for the FhbB-FH interaction in complement evasion and serum sensitivity had not been demonstrated. Here we assess the serum resistance of T. denticola strain 35405 (Td35405wt) and isogenic mutants deficient in dentilisin (Td35405-CCE) and FhbB production (Td35405ΔfhbB), respectively. Both dentilisin and FhbB have been postulated to be key virulence factors that mediate complement evasion. Consistent with conditions in the subgingival crevice, an environment with a significant concentration of complement, Td35405wt was resistant to serum concentrations as high as 25%. Deletion of fhbB (Td35405ΔfhbB), which resulted in the complete loss of FH binding ability, but not inactivation of dentilisin activity (Td35405-CCE), rendered T. denticola highly sensitive to 25% human serum with 80% of the cells being disrupted after 4 h of incubation. Heat treatment of the serum to inactivate complement confirmed that killing was mediated by complement. These results indicate that the FH-FhbB interaction is required for serum resistance whereas dentilisin is not. This report provides new insight into the novel complement evasion mechanisms of T. denticola.
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.