ArticleThe Journal of experimental medicine2023
Neutrophil extracellular traps and extracellular histones potentiate IL-17 inflammation in periodontitis.
Article in The Journal of experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 1 of them a synthesis that pooled it.
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Who cites it
98 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.
- Association Between IL-17 and Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-Analysis.International journal of chronic obstructive pulmonary disease · 2023Pooled it
- Microneedle-based injection of Fungizone/Amphotericin B: an effective treatment for American cutaneous leishmaniasis in mice.Drug delivery · 2026Article
- The dynamic landscape of T helper cell plasticity and Th17-Treg instability in periodontitis.Experimental & molecular medicine · 2026Review
- Apical Periodontitis May Exacerbate Ulcerative Colitis via Neutrophil Extracellular Trap-Mediated Systemic Inflammation and Intestinal Barrier Disruption in Mice.International endodontic journal · 2026Article
- Role of post-translational modifications in modulating histone reactivity in the extracellular environment.Biochemical Society transactions · 2026Review
- Gut microbiota transmits osteoimmune dysregulation and exacerbates trabecular bone loss in tristetraprolin-deficient mice.Journal of bone and mineral metabolism · 2026Article
- Spatiotemporal immunomodulation with programmable biomaterials to promote musculoskeletal tissue regeneration.Bioactive materials · 2026Review
- Macrophages Intracellularly Gelated With Bioactive Hydrogels for Synergistic Neutralization, Eradication, and Osteopromotion in Periodontitis Treatment.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Neutrophil extracellular traps in osteoporosis: mechanistic links to bone remodeling imbalance and therapeutic perspectives.Molecular biology reports · 2026Review
- Turmeric-derived nanovesicles reprogram pathological NETosis to mitigate inflammatory bone loss.Journal of nanobiotechnology · 2026Article
- Rosavin alleviates COPD via inhibition of IL-17-enriched NET formation and NF-κB signaling.Biology direct · 2026Article
- Mechanisms underlying pyogenic bacterial infections of the skin.Archives of microbiology · 2026Review
- From Gene Expression to Candidate Biomarkers in Ulcerative Colitis: Aquaporin-9 in Neutrophil Extracellular Traps Formation Pathways.Iranian journal of medical sciences · 2026Article
- Th17/IL-17A Drives Alveolar Bone Loss via the JAK/STAT3-RANKL Axis in the Periodontal Ligament.Oral diseases · 2026Article
- Myeloid-Derived Grancalcin Promotes Periodontal Inflammation and Pathological Bone Remodeling in Periodontitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Tissue-specific adaptation of human T cells is preserved during tissue inflammation.bioRxiv : the preprint server for biology · 2026Article
- Single-Cell Analysis of Fibroblast Subpopulations in Skin and Oral Mucosa.Journal of dental research · 2026Review
- Modulation of the Immune-Inflammatory Microenvironment by Implant Material Properties in Peri-Implantitis.International journal of molecular sciences · 2026Review
- Periodontitis and Chronic Liver Disease: Mechanistic Insights Focusing onMicroorganisms · 2026Review
- Mucosal Inflammation Shapes Human Neutrophil States in Tissue and Circulation.bioRxiv : the preprint server for biology · 2026Article
38 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Neutrophil infiltration is a hallmark of periodontitis, a prevalent oral inflammatory condition in which Th17-driven mucosal inflammation leads to destruction of tooth-supporting bone. Herein, we document that neutrophil extracellular traps (NETs) are early triggers of pathogenic inflammation in periodontitis. In an established animal model, we demonstrate that neutrophils infiltrate the gingival oral mucosa at early time points after disease induction and expel NETs to trigger mucosal inflammation and bone destruction in vivo. Investigating mechanisms by which NETs drive inflammatory bone loss, we find that extracellular histones, a major component of NETs, trigger upregulation of IL-17/Th17 responses, and bone destruction. Importantly, human findings corroborate our experimental work. We document significantly increased levels of NET complexes and extracellular histones bearing classic NET-associated posttranslational modifications, in blood and local lesions of severe periodontitis patients, in the absence of confounding disease. Our findings suggest a feed-forward loop in which NETs trigger IL-17 immunity to promote immunopathology in a prevalent human inflammatory disease.
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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.