title: Effects of chitosan particles in periodontal pathogens and gingival fibroblasts.
abstract: Chitosan is a naturally derived polymer with antimicrobial and anti-inflammatory properties. However, studies evaluating the role of chitosan in the control of periodontal pathogens and the responses of fibroblasts to inflammatory stimuli are lacking. In the present study, we analyzed whether chitosan particles may inhibit the growth of periodontal pathogens and modulate the inflammatory response in human gingival fibroblasts. Chitosan particles were generated through ionic gelation. They inhibited the growth of Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans at 5 mg/mL. Conversely, IL-1β strongly stimulated PGE2 protein levels in gingival fibroblasts, and chitosan inhibited this response at 50 µg/mL. IL-1β-stimulated PGE2 production was dependent on the JNK pathway, and chitosan strongly inhibited this response. IL-1β stimulated NF-κB activation, another signaling pathway involved in PGE2 production. However, chitosan particles were unable to modify NF-κB signaling. The present study shows that chitosan exerts a predominantly anti-inflammatory activity by modulating PGE2 levels through the JNK pathway, which may be useful in the prevention or treatment of periodontal inflammation.
authors.affiliation: Dentistry Academic Unit, Faculty of Medicine, Pontificia Universidad Católica de Chile.
authors.forename: R
authors.initials: R
authors.lastname: Arancibia
authors.forename: C
authors.initials: C
authors.lastname: Maturana
authors.forename: D
authors.initials: D
authors.lastname: Silva
authors.forename: N
authors.initials: N
authors.lastname: Tobar
authors.forename: C
authors.initials: C
authors.lastname: Tapia
authors.forename: J C
authors.initials: JC
authors.lastname: Salazar
authors.forename: J
authors.initials: J
authors.lastname: Martínez
authors.forename: P C
authors.initials: PC
authors.lastname: Smith
mesh_terms: D000328:Adult; D016976:Aggregatibacter actinomycetemcomitans / Q000187:drug effects*; D000873:Anthracenes / Q000494:pharmacology; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001431:Bacteriological Techniques; D002470:Cell Survival; D002478:Cells, Cultured; D048271:Chitosan / Q000494:pharmacology*; D015232:Dinoprostone / Q000037:antagonists & inhibitors; D005347:Fibroblasts / Q000187:drug effects; D005881:Gingiva / Q000166:cytology / Q000187:drug effects*; D006801:Humans; D007202:Indicators and Reagents; D053583:Interleukin-1beta / Q000494:pharmacology; D048031:JNK Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors; D007770:L-Lactate Dehydrogenase / Q000032:analysis; D020935:MAP Kinase Signaling System / Q000187:drug effects; D016328:NF-kappa B / Q000187:drug effects; D053758:Nanoparticles; D010510:Periodontal Diseases / Q000382:microbiology; D010766:Phosphorylation; D016966:Porphyromonas gingivalis / Q000187:drug effects*; D015398:Signal Transduction / Q000187:drug effects; D013778:Tetrazolium Salts; D013844:Thiazoles; D051996:Transcription Factor RelA / Q000187:drug effects
chemical_list: D000873:Anthracenes; D000900:Anti-Bacterial Agents; D000893:Anti-Inflammatory Agents; D007202:Indicators and Reagents; D053583:Interleukin-1beta; D016328:NF-kappa B; D013778:Tetrazolium Salts; D013844:Thiazoles; D051996:Transcription Factor RelA; C070380:3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium; C432165:pyrazolanthrone; D048271:Chitosan; D007770:L-Lactate Dehydrogenase; D048031:JNK Mitogen-Activated Protein Kinases; D015232:Dinoprostone
keywords: Aggregatibacter actinomycetemcomitans; Porphyromonas gingivalis; biomaterials; inflammation; periodontal diseases; periodontitis