3-(4-5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2h-tetrazolium and pyrazolanthrone

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.

Topics: Adult; Aggregatibacter actinomycetemcomitans; Anthracenes; Anti-Bacterial Agents; Anti-Inflammatory Agents; Bacteriological Techniques; Cell Survival; Cells, Cultured; Chitosan; Dinoprostone; Fibroblasts; Gingiva; Humans; Indicators and Reagents; Interleukin-1beta; JNK Mitogen-Activated Protein Kinases; L-Lactate Dehydrogenase; MAP Kinase Signaling System; Nanoparticles; NF-kappa B; Periodontal Diseases; Phosphorylation; Porphyromonas gingivalis; Signal Transduction; Tetrazolium Salts; Thiazoles; Transcription Factor RelA