Chitosan-triclosan particles modulate inflammatory signaling in gingival fibroblasts
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2018-04Metadata
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Pavez, L.
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Chitosan-triclosan particles modulate inflammatory signaling in gingival fibroblasts
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Background and Objectives: An important goal of periodontal therapy is the modulation of the inflammatory response. To this end, several pharmacological agents have been evaluated. Triclosan corresponds to an antibacterial and anti-inflammatory agent currently used in periodontal therapy. Chitosan is a natural polymer that may act as a drug delivery agent and exerts antibacterial and anti-inflammatory activities. Therefore, an association between both molecules might be useful to prevent inflammation and tissue destruction in periodontal tissues.
Material and Methods: In the present study, we have generated chitosan-triclosan particles and evaluated their morphology, charge, biocompatibility and gene expression analysis in human gingival fibroblasts.
Results: The chitosan-triclosan particles size and Z potential were 129 +/- 47 nm and 51 +/- 17 mV respectively. Human gingival fibroblast viability was not affected by chitosan-triclosan. A total of 1533 genes were upregulated by interleukin (IL)-1 beta. On the other hand, 943 were downregulated in fibroblasts stimulated with IL-1 beta plus chitosan-triclosan particles. Fifty-one genes were identified as molecular targets upregulated by IL-1 beta and downregulated by the chitosan-triclosan particles. The gene ontology analysis revealed that these genes were enriched in categories related to biological processes, molecular function and cellular components. Furthermore, using real-time reverse transcription-polymerase chain reaction beta-actin, fibronectin, inter-leukin-6 and IL-1b genes were confirmed as targets upregulated by IL-1 beta and downregulated by chitosan-triclosan particles.
Conclusion: Our results show that chitosan-triclosan particles are able to modulate the inflammatory response in gingival fibroblasts. This effect might be useful in the prevention and/or treatment of inflammation in periodontal diseases.
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Chilean Fund for Science and Development FONDEF
DO8I1141
Colgate-Palmolive Chile
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J Periodont Res. 2018;53:232–239
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