ArticleJournal of immunology research2025
The Dynamic Expression Changes of Neutrophil Extracellular Traps in Mouse Apical Periodontitis: A Potential Correlation With IL-17.
Article in Journal of immunology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Apical Periodontitis May Exacerbate Ulcerative Colitis via Neutrophil Extracellular Trap-Mediated Systemic Inflammation and Intestinal Barrier Disruption in Mice.International endodontic journal · 2026Article
- The Dynamic Expression Changes of Neutrophil Extracellular Traps in Mouse Apical Periodontitis: A Potential Correlation With IL-17.Journal of immunology research · 2025Article
- Clinical updates of JAK inhibitors in cutaneous granulomatous diseases.Frontiers in immunology · 2025Review
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Authors and funding
8 authors.
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Abstract
Neutrophil extracellular traps (NETs) consist of decondensed chromatin and antimicrobial proteins, which are released from neutrophils and have been implicated in several inflammatory diseases. NETs and interleukin (IL)-17 constitute a feed-forward loop that promotes immunopathological development of inflammation. Therefore, this study aimed to investigate the dynamic distribution of NETs and their colocalization with IL-17 during the progression of apical periodontitis in established mouse models. Apical periodontitis was induced in mice by exposing the pulp of the mandibular first molars, with mandibles harvested on day 0, 7, 14, 21, and 28 after pulp exposure. Micro-CT and high-resolution X-ray scanning showed progressive increases in both the area and volume of periapical lesions from day 0 to day 28. Osteoclasts in the periapical lesions were identified using tartrate-resistant acid phosphatase (TRAP) staining, with their numbers peaking on day 21. Immunofluorescence staining was performed for citrullinated histone H3 (CitH3), myeloperoxidase (MPO), neutrophil elastase (NE), and IL-17 to localize NETs and their colocalization with IL-17 in lesions. NETs, which were visible on day 7 and increased gradually until day 21, primarily located in inflammatory infiltration areas of the periapical tissue. Additionally, western blot analysis showed increased CitH3 expression in periapical lesions on day 21 after pulp exposure, further confirming the presence of NETs. Both RT-qPCR and enzyme-linked immunosorbent assay (ELISA) revealed increased IL-17 expression in periapical lesions. The colocalization of CitH3, the major component of NETs and IL-17 peaked on day 21 after pulp exposure. Furthermore, in vitro experiments demonstrated that IL-17 promoted NETs formation under lipopolysaccharide (LPS)-simulated inflammatory conditions. Our findings indicated that NETs expression changed dynamically and suggested a feedback loop between NETs and IL-17 during the development of apical periodontitis in mouse models.
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