ArticleInfection and immunity2009
Involvement of Toll-like receptors 2 and 4 in the innate immune response to Treponema denticola and its outer sheath components.
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 37 papers, 1 of them a synthesis that pooled it.
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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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Assessing the Impact of Stem Cell-based Therapy on Periodontal Health: A Meta-analysis of Clinical Studies.Current stem cell research & therapy · 2025Pooled it
- Oxidized Low-Density Lipoprotein Enhances Toll-like Receptor-Mediated Osteoclastogenic Responses in the Absence of Exogenous RANKL: Implications for Inflammatory Osteoclastogenesis in Periodontitis.Medicina (Kaunas, Lithuania) · 2026Article
- Hyperbaric oxygen protects against periodontal bone loss by modulating inflammation and bone remodeling via RANKL/OPG expression in ligature-induced periodontitis.International journal of medical sciences · 2026Article
- Neutrophil-derived oncostatin m contributes to endothelial cell dysfunction during Treponema denticola interaction.PloS one · 2026Article
- Treponema denticola major surface protein (Msp): a key player in periodontal pathogenicity and immune evasion.Archives of microbiology · 2025Review
- Outer Membrane Vesicles Derived from Oral Bacteria Act as a Dagger in Host Immunity: Insight Tips from Local Diseases to Systemic Effects.International journal of biological sciences · 2025Review
- Oral SpirocheteInternational journal of molecular sciences · 2023Article
- Periodontal Pathogens and Their Links to Neuroinflammation and Neurodegeneration.Microorganisms · 2023Review
- Periodontitis as a promoting factor of T2D: current evidence and mechanisms.International journal of oral science · 2023Review
- Macrophages in periodontitis: A dynamic shift between tissue destruction and repair.The Japanese dental science review · 2022Review
- Activation of bone marrow-derived dendritic cells and CD4Journal of oral microbiology · 2022Article
- Paradigm shift in the pathogenesis and treatment of oral cancer and other cancers focused on the oralome and antimicrobial-based therapeutics.Periodontology 2000 · 2021Review
- Approaches to Understanding Mechanisms of Dentilisin Protease Complex Expression inFrontiers in cellular and infection microbiology · 2021Review
- Infection and atherosclerosis: TLR-dependent pathways.Cellular and molecular life sciences : CMLS · 2020Review
- How the evolving epidemics of opioid misuse and HIV infection may be changing the risk of oral sexually transmitted infection risk through microbiome modulation.Critical reviews in microbiology · 2020Review
- The Msp Protein of Treponema denticola Interrupts Activity of Phosphoinositide Processing in Neutrophils.Infection and immunity · 2019Article
- Diet-induced Generalized Periodontitis in Lewis Rats.Comparative medicine · 2019Article
- Outer Membrane Vesicle-Host Cell Interactions.Microbiology spectrum · 2019Article
- Review
- A Differential Innate Immune Response in Active and Chronic Stages of Bovine Infectious Digital Dermatitis.Frontiers in microbiology · 2018Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Treponema denticola is considered an important oral pathogen in the development and progression of periodontal diseases. In the present study, the mechanisms of recognition and activation of murine macrophages by T. denticola and its major outer sheath protein (MSP) and lipooligosaccharide (LOS or glycolipid) were investigated. T. denticola cells and the MSP induced innate immune responses through TLR2-MyD88, whereas LOS induced a macrophage response through TLR4-MyD88. The presence of gamma interferon (IFN-gamma), or of high numbers of T. denticola, circumvented the requirement for TLR2 for the macrophage response to T. denticola, although the response was still dependent on MyD88. In contrast, synergy with IFN-gamma did not alter the TLR dependence of the response to the T. denticola surface components LOS and MSP, despite enhanced sensitivity. These data suggest that although there is flexibility in the requirements for recognition of T. denticola cells (TLR2 dependent or independent), MyD88 is a requirement for the downstream signaling events that lead to inflammation. We also demonstrate that both outer sheath molecules LOS and MSP induce macrophage tolerance to further stimulation with enterobacterial lipopolysaccharide. Tolerance induced by T. denticola components during mixed infections may represent a general mechanism through which bacteria evade clearance.
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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.