ArticleInfection and immunity2007
Differential activation of human gingival epithelial cells and monocytes by Porphyromonas gingivalis fimbriae.
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 44 papers, 1 of them a synthesis that pooled it.
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
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
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- The prevalence of fimA genotypes of Porphyromonas gingivalis in patients with chronic periodontitis: A meta-analysis.PloS one · 2020Pooled it
- The Role of Caspase-1 and Caspase-4 in Modulating Gingival Epithelial Cell Responses toPathogens (Basel, Switzerland) · 2025Article
- Alzheimer's Disease andLife (Basel, Switzerland) · 2025Review
- Frankincense (Current issues in molecular biology · 2024Article
- Potential role of epithelial-mesenchymal transition induced by periodontal pathogens in oral cancer.Journal of cellular and molecular medicine · 2024Review
- MicroRNAs and Periodontal Disease: Helpful Therapeutic Targets?Advanced pharmaceutical bulletin · 2023Review
- Phylogenomic analysis of theFrontiers in microbiology · 2023Article
- Porphyromonas gingivalis Virulence Factors and Clinical Significance in Periodontal Disease and Coronary Artery DiseasesPathogens (Basel, Switzerland) · 2022Review
- Complement Is Required for Microbe-Driven Induction of Th17 and Periodontitis.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Review
- Ginsenoside Rb3 Inhibits Pro-Inflammatory Cytokines via MAPK/AKT/NF-κB Pathways and Attenuates Rat Alveolar Bone Resorption in Response toMolecules (Basel, Switzerland) · 2020Article
- Current understanding of periodontal disease pathogenesis and targets for host-modulation therapy.Periodontology 2000 · 2020Review
- Polymeric Carriers for Delivery Systems in the Treatment of Chronic Periodontal Disease.Polymers · 2020Review
- Article
- Roles of Porphyromonas gingivalis and its virulence factors in periodontitis.Advances in protein chemistry and structural biology · 2020Review
- Biofilm-stimulated epithelium modulates the inflammatory responses in co-cultured immune cells.Scientific reports · 2019Article
- Article
- Pathogenesis of Important Virulence Factors ofFrontiers in cellular and infection microbiology · 2019Review
- Complement-Dependent Mechanisms and Interventions in Periodontal Disease.Frontiers in immunology · 2019Review
- Activation of the Innate Immune System by Treponema denticola Periplasmic Flagella through Toll-Like Receptor 2.Infection and immunity · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Humans develop periodontitis in response to challenge by microbial dental plaque. Inflammation begins after perturbation of gingival epithelial cells by subgingival bacteria interacting through pattern-recognition receptors, including the Toll-like receptors (TLR). Porphyromonas gingivalis is a major periodontopathogen that interacts with epithelial cells through its cell surface fimbriae (FimA), leading to colonization and/or invasion. Previous work by our group has established membrane CD14 as an essential coreceptor for TLR2-mediated activation of transfected cell lines by P. gingivalis FimA. We have shown that gingival epithelial cells express TLR2 but not CD14 on their cell surfaces. We thus speculated that P. gingivalis FimA does not readily activate epithelial innate immune responses but rather functions to promote P. gingivalis colonization in the absence of a vigorous FimA-induced response. This hypothesis was verified by the findings that primary human gingival epithelial cells responded poorly to FimA in terms of interleukin (IL)-6, IL-8, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor alpha responses, in stark contrast to the marked response to other TLR2 agonists (Pam3Cys, FSL-1) that are not strictly dependent on CD14. On the other hand, CD14-expressing human primary monocytes responded with high levels of the same cytokines to both FimA and the control TLR2 agonists. The gingival epithelial cells failed to respond to FimA even in the presence of exogenously added soluble CD14. These data indicate that the gingival epithelial cell hyporesponsiveness to FimA is attributable to the lack of membrane-expressed but not soluble CD14. In conclusion, P. gingivalis FimA differentially activates human monocytes and epithelial cells, perhaps reflecting different tactics used by P. gingivalis when interacting with different host cell types or a host strategy to limit inflammation.
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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.