Dentistry Academic Unit, Faculty of Medicine, Pontificia Universidad Católica de Chile.
J Dent Res. 2013 Aug;92(8):740-5. doi: 10.1177/0022034513494816. Epub 2013 Jun 20.
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.
壳聚糖是一种具有抗菌和抗炎特性的天然衍生聚合物。然而,目前尚缺乏评估壳聚糖在控制牙周病原体和纤维母细胞对炎症刺激反应中的作用的研究。在本研究中,我们分析了壳聚糖颗粒是否可以抑制牙周病原体的生长并调节人牙龈成纤维细胞的炎症反应。壳聚糖颗粒通过离子凝胶形成。它们在 5mg/mL 时抑制牙龈卟啉单胞菌和伴放线放线杆菌的生长。相反,IL-1β 强烈刺激牙龈成纤维细胞中 PGE2 蛋白水平,而壳聚糖在 50μg/mL 时抑制该反应。IL-1β 刺激 PGE2 产生依赖于 JNK 途径,壳聚糖强烈抑制该反应。IL-1β 刺激 NF-κB 激活,这是另一种参与 PGE2 产生的信号通路。然而,壳聚糖颗粒不能改变 NF-κB 信号。本研究表明,壳聚糖通过调节 JNK 途径中的 PGE2 水平发挥主要的抗炎作用,这可能有助于预防或治疗牙周炎。