ArticleImmunology and cell biology2015
GM-CSF and uPA are required for Porphyromonas gingivalis-induced alveolar bone loss in a mouse periodontitis model.
Article in Immunology and cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Polymicrobial-driven NLRP6 inflammasome regulates IL-1β production and alveolar bone loss in a murine model of periodontitis.PLoS pathogens · 2026Article
- The Role of Lacticaseibacillus Rhamnosus in Periodontitis Management: From Microecological Regulation to Clinical Application.Probiotics and antimicrobial proteins · 2026Review
- Evaluating the Efficacy of Sequential Microimmunotherapy Medicine on Early and Established Postmenopausal Osteoporosis Rat Model.Journal of osteoporosis · 2026Article
- Association Between Circulating Inflammatory Cytokines and Dentofacial Anomalies.International dental journal · 2025Article
- A Sequential Micro-Immunotherapy Medicine Increases Collagen Deposition in Human Gingival Fibroblasts and in an Engineered 3D Gingival Model under Inflammatory Conditions.International journal of molecular sciences · 2023Article
- Lactobacilli Attenuate the Effect ofFrontiers in microbiology · 2022Article
- Granulocyte-macrophage colony-stimulating factor (GM-CSF) in subjects with different stages of periodontitis according to the new classification.Journal of applied oral science : revista FOB · 2022Article
- Tuning cytokines enriches dendritic cells and regulatory T cells in the periodontium.Journal of periodontology · 2020Article
- GM-CSF in inflammation.The Journal of experimental medicine · 2020Review
- Plasmin inhibition by bacterial serpin: Implications in gum disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Age and Periodontal Health - Immunological View.Current oral health reports · 2018Article
- Anti-colony-stimulating factor therapies for inflammatory and autoimmune diseases.Nature reviews. Drug discovery · 2016Review
- Transcriptome Analysis of B Cell Immune Functions in Periodontitis: Mucosal Tissue Responses to the Oral Microbiome in Aging.Frontiers in immunology · 2016Article
- Porphyromonas gingivalis-derived RgpA-Kgp Complex Activates the Macrophage Urokinase Plasminogen Activator System: IMPLICATIONS FOR PERIODONTITIS.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Granulocyte-macrophage colony-stimulating factor (GM-CSF) and urokinase-type plasminogen activator (uPA) can contribute to the progression of chronic inflammatory diseases with possible involvement of macrophages. In this study, we investigated the role of both GM-CSF and uPA in Porphyromonas gingivalis-induced experimental periodontitis using GM-CSF-/- and uPA-/- mice. Intra-oral inoculation of wild-type (WT) C57BL/6 mice with P. gingivalis resulted in establishment of the pathogen in plaque and a significant increase in alveolar bone resorption. The infected mice also exhibited a CD11b(+) CD86(+) macrophage infiltrate into the gingival tissue, as well as P. gingivalis-specific pro-inflammatory cytokine and predominantly IgG2b antibody responses. In comparison, intra-oral inoculation of P. gingivalis did not induce bone resorption and there was significantly less P. gingivalis recovered from plaque in GM-CSF-/- and uPA-/- mice. Furthermore, P. gingivalis did not induce a macrophage gingival infiltrate or activate isolated peritoneal macrophages from the gene-deficient mice. Pro-inflammatory P. gingivalis-specific T-cell cytokine responses and serum interferon-gamma (IFN-γ) and IgG2b concentrations were significantly lower in GM-CSF-/- mice. In uPA-/- mice, T-cell responses were lower but serum IFN-γ and IgG2b levels were comparable with WT mice levels. These results suggest that GM-CSF and uPA are both involved in the progression of experimental periodontitis, possibly via a macrophage-dependent mechanism(s).
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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.