ArticleJournal of applied oral science : revista FOB2022
Macrophage M1 polarization mediated via the IL-6/STAT3 pathway contributes to apical periodontitis induced by Porphyromonas gingivalis.
Article in Journal of applied oral science : revista FOB, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 45 citations in OpenAlex.
- M2 polarization of macrophages: Manipulation of spinal cord injury repair.Neural regeneration research · 2026Article
- IRF2 exacerbates diabetic neuropathic pain by promoting high glucose-induced M1 polarization through IL-6/STAT3.Genes & genomics · 2026Article
- Article
- Age-Associated Senescence of Decidual Macrophages: A Key Mediator of Adverse Pregnancy Outcomes in Advanced Maternal Age.Aging cell · 2026Article
- Immunotherapies based on macrophage reprogramming in periodontitis and apical periodontitis.Clinical oral investigations · 2026Review
- Nell-1 inhibits osteoclast differentiation and bone resorption in apical periodontitis.Journal of molecular histology · 2026Article
- Porphyromonas gingivalis promotes oral squamous cell carcinoma progression via the IL-6/EZH2/Snai2 axis.Scientific reports · 2026Article
- Inflammatory bone loss and signaling pathways in periodontitis: mechanistic insights and emerging therapeutic strategies.Bone research · 2026Review
- Impact of anti-TNF and anti-IL-12/IL-23 antibody therapy on periodontal inflammation and gingival crevicular fluid IL-6 in patients with inflammatory bowel diseases.Frontiers in immunology · 2026Article
- Periodontal disease and endocrine imbalance: a molecular pathways perspective.Frontiers in dental medicine · 2026Review
- Targeting innate immunity to modulate bone metabolism: a novel strategy for osteoporosis treatment.Frontiers in aging · 2026Review
- Molecular cytokine-dependent mechanisms of periodontitis pathogenesis and the potential for pharmacological IL-1 modulation in disease treatment.Frontiers in dental medicine · 2026Review
- PPAR-γ Inhibits Chronic Apical Periodontitis by Facilitating Macrophage Efferocytosis.International journal of molecular sciences · 2025Article
- Transcriptional regulation of human follicular dendritic cell-secreted protein gene by interleukin-6.Odontology · 2025Article
- Fracture-Induced Immunological Cascades Trigger Rapid Systemic Bone Loss via Osteocyte-Regulated Osteoclastogenesis.ImmunoTargets and therapy · 2025Article
- Chemokine receptor-2 deficiency induced mild experimental periapical lesion in mice.Journal of dental sciences · 2025Article
- Selective Glycopolymer Inhibitors of Galectin-3: Supportive Anti-Cancer Agents Protecting Monocytes and Preserving Interferon-Gamma Function.International journal of nanomedicine · 2025Article
- Disruption of CDK5 regulatory subunit 1, p35, limits immunosuppressive M2 macrophages while maintaining functional M1 macrophages.Frontiers in immunology · 2025Article
- The Effects and Mechanisms of Patchouli Alcohol on Experimental Periodontitis Rats Based on the OPG/RANK/RANKL/P38 MAPK Signaling Pathway.Journal of inflammation research · 2025Article
- Macrophage Metabolic Reprogramming in Inflammatory Bowel Diseases: From Pathogenesis to Therapy.Journal of inflammation research · 2025Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the involvement of IL-6/STAT3 signaling pathway activation in macrophage polarization and bone destruction related to apical periodontitis (AP) stimulated by Porphyromonas gingivalis. METHODOLOGY: Macrophage polarization, IL-6/STAT3 expression, and the presence of P. gingivalis were detected in human AP tissues via RT-qPCR, western blotting, and immunohistochemistry staining. Murine bone marrow derived macrophages were isolated and cultured with P. gingivalis W83 in vitro, and levels of macrophage IL-6 expression, STAT3 phosphorylation, and macrophage polarization with or without the selective STAT3 phosphorylation inhibitor Stattic (5 μM) were detected via ELISA, western blotting, RT-qPCR, and flow cytometry, respectively. P. gingivalis-induced murine AP models were constructed, and bone destruction and macrophage polarization in the apical region were evaluated. Transwell co-culture systems were used to investigate the effects of macrophages infected with P. gingivalis on osteogenesis and osteoclastogenesis.
resultsP. gingivalis was detected in human AP tissues that highly expressed IL-6/STAT3, and the M1 subtype of macrophages was more abundant in these tissues. P. gingivalis infection induced IL-6 expression, STAT3 phosphorylation, and M1 polarization of macrophages, while 5 μM of Stattic partially abolished these activation effects. Systemic STAT3 blockade via oral administration of Stattic at a dose of 25 mg kg-1 alleviated murine periapical bone resorption and apical infiltration of M1 macrophages induced by P. gingivalis infection in vivo. Furthermore, macrophages infected with P. gingivalis promoted bone destruction via secretion of IL-6, TNF-α, and RANKL, which hinder pre-osteoblast expression of Runx2 and accelerate pre-osteoclast expression of NFAT2.
conclusionsThe activation of IL-6/STAT3 signaling pathway is involved in mediating macrophages M1 polarization in the P. gingivalis induced apical inflammatory context and may also be intimately involved in the bone loss caused by P. gingivalis infection, directing the M1 macrophage infiltration during the progression of AP.
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