Anti‐inflammation effects of injectable platelet‐rich fibrin via macrophages and dendritic cells

Immune response to implantation materials plays a critical role during early local inflammation and biomaterial‐induced regeneration or restoration. A novel platelet concentrate termed i‐PRF (injectable platelet‐rich fibrin) has recently been developed without any additives by low centrifugation spe...

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Bibliographic Details
Published in:Journal of biomedical materials research. Part A 2020-01, Vol.108 (1), p.61-68
Main Authors: Zhang, Jinglun, Yin, Chengcheng, Zhao, Qin, Zhao, Zifan, Wang, Jinyang, Miron, Richard J., Zhang, Yufeng
Format: Article
Language:English
Subjects:
Additives
anti‐inflammation effects
Biomaterials
Biomedical materials
Centrifugation
Dendritic cells
Fibrin
Growth factors
Immune response
Immune system
Implantation
Inflammation
Inflammatory response
i‐PRF
Lipopolysaccharides
Macrophages
Muscles
Phenotypes
Platelets
Regeneration
Restoration
Surgical implants
TLR4 protein
Toll-like receptors
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Summary:Immune response to implantation materials plays a critical role during early local inflammation and biomaterial‐induced regeneration or restoration. A novel platelet concentrate termed i‐PRF (injectable platelet‐rich fibrin) has recently been developed without any additives by low centrifugation speeds. To date, scientists have investigated the capability of releasing growth factors to improve regeneration but have ignored whether i‐PRF can inhibit the inflammatory effect around the wound. The present study investigated the anti‐inflammation effects of i‐PRF on immune response‐related cells, especially macrophages and dendric cells. We found that i‐PRF reduced pro‐inflammatory M1 phenotype of macrophages and activated dendritic cells around muscle defect that was injected with bacterial suspension. Moreover, in vitro experiments showed similar results. i‐PRF deleted inflammatory response caused by lipopolysaccharide to some extent. We determined that TLR4, an activator of inflammatory stimulation and p‐p65, a key factor belongs to classical inflammatory related NF‐κB signal pathway, can be inhibited by use of i‐PRF. Results indicate the potential anti‐inflammatory role of i‐PRF during regeneration and restoration.
ISSN:1549-3296
1552-4965
DOI:10.1002/jbm.a.36792