ArticlePathogens and disease2016
Macrophage polarization in response to oral commensals and pathogens.
Article in Pathogens and disease, 2016. 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
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
27 citing papers in PubMed, 49 citations in OpenAlex.
- Commensal microbiota-coated biohybrid implants induce antibiofilm, osteogenic, and immunomodulatory responses in a human 3D immunocompetent model.Bioactive materials · 2026Article
- Dicer-independent miR-451a is upregulated in periodontitis and potentiates inflammation by impairing macrophage polarization and SOCS activity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Polymicrobial-driven NLRP6 inflammasome regulates IL-1β production and alveolar bone loss in a murine model of periodontitis.PLoS pathogens · 2026Article
- A CRISPR array orchestrates virulence and host response inMicrobiology spectrum · 2026Article
- Harnessing Microbiome-Mediated and Macrophage-Driven Mechanisms for Oral Wound Healing.Microorganisms · 2026Review
- Harnessing the Therapeutic Potential of Extracellular Vesicles for Oral Wound Healing.Bioengineering (Basel, Switzerland) · 2026Review
- Macrophage dynamics and the role of TREM2 at the oral mucosal barrier.Journal of translational medicine · 2025Article
- Ferroptosis in periodontitis: mechanisms, impacts, and systemic connections.Cell death discovery · 2025Review
- Development of a Coculture Model for Assessing Competing Host Mammalian Cell and Bacterial Attachment on Zirconia versus Titanium.ACS biomaterials science & engineering · 2024Article
- Oral microbiota-host interaction: the chief culprit of alveolar bone resorption.Frontiers in immunology · 2024Review
- Article
- Discovery of phosphorylated lantibiotics with proimmune activity that regulate the oral microbiome.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Macrophages in periodontitis: A dynamic shift between tissue destruction and repair.The Japanese dental science review · 2022Review
- Interleukin-34 permits Porphyromonas gingivalis survival and NF-κB p65 inhibition in macrophages.Molecular oral microbiology · 2022Article
- Cellular Mechanisms of Inflammaging and Periodontal Disease.Frontiers in dental medicine · 2022Article
- Macrophage M1 polarization mediated via the IL-6/STAT3 pathway contributes to apical periodontitis induced by Porphyromonas gingivalis.Journal of applied oral science : revista FOB · 2022Article
- Human and herpesvirus microRNAs in periodontal disease.Periodontology 2000 · 2021Review
- Maintaining homeostatic control of periodontal bone tissue.Periodontology 2000 · 2021Review
- Dysbiosis From a Microbial and Host Perspective Relative to Oral Health and Disease.Frontiers in microbiology · 2021Review
- Innate Phagocyte Polarization in the Oral Cavity.Frontiers in immunology · 2021Review
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
Macrophages have been identified in the periodontium. Data have phenotypically described these cells, demonstrated changes with progressing periodontal disease, and identified their ability to function in antigen-presentation critical for adaptive immune responses to individual oral bacterium. Recent evidence has emphasized an important role for the plasticity of macrophage phenotypes, not only in the resulting function of these cells in various tissues, but also clear differences in the stimulatory signals that result in M1 (classical activation, inflammatory) and M2 (alternative activation/deactivated, immunomodulatory) cells. This investigation hypothesized that the oral pathogens, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans induce M1-type cells, while oral commensal bacteria primarily elicit macrophage functions consistent with an M2 phenotype. However, we observed that the M1 output from P. gingivalis challenge, showed exaggerated levels of pro-inflammatory cytokines, with a much lower production of chemokines related to T-cell recruitment. This contrasted with A. actinomycetemcomitans infection that increased both the pro-inflammatory cytokines and T-cell chemokines. Thus, it appears that P. gingivalis, as an oral pathogen, may have a unique capacity to alter the programming of the M1 macrophage resulting in a hyperinflammatory environment and minimizing the ability for T-cell immunomodulatory influx into the lesions.
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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.