Abstract
Chronic inflammation is a pathological process where cells of the mesenchymal lineage become a major source of inflammatory mediators. Platelet-rich fibrin (PRF) has been shown to possess potent anti-inflammatory activity in macrophages, but its impact on mesenchymal cells has not been investigated. The aim of this study was, therefore, to expose mesenchymal cells to inflammatory cytokines together with lysates generated from liquid platelet-poor plasma (PPP), the cell-rich buffy coat layer (BC; concentrated-PRF or C-PRF), and the remaining red clot layer (RC), following centrifugation of blood. Heating PPP generates an albumin gel (Alb-gel) that when mixed back with C-PRF produces Alb-PRF. Membranes prepared from solid PRF were also subjected to lysis. We report here that lysates of PPP, BC, and PRF decreased the cytokine-induced expression of interleukin 6 (IL6) and nitric oxide synthase (iNOS) in the bone marrow-derived ST2 cells. Consistently, PPP, BC, and PRF greatly decreased the phosphorylation and nuclear translocation of p65 in ST2 cells. The inflammatory response caused by Pam3CSK4 was reduced accordingly. Moreover, PPP, BC, and PRF reduced the enhanced expression of inflammatory mediators IL6 and iNOS in 3T3-L1 pre-adipocyte mesenchymal cells, and iNOS and CCL5 in murine calvarial cells. Surprisingly, PRF lysates were not effective in reducing the inflammatory response of human gingival fibroblasts and HSC2 epithelial cells. The data from the present study suggest that both liquid PRF and solid PRF exert potent anti-inflammatory activity in murine mesenchymal cells.
Highlights
Chronic inflammatory diseases share a conserved pathological mechanism where the immune response fails to remove the detrimental agents, and the resolution of inflammation is hampered [1,2,3]
We have recently shown that it is in particular the platelet-poor plasma (PPP), buffy coat layer (BC), and Platelet-rich fibrin (PRF) lysates that greatly suppress the inflammatory response of macrophages in vitro [26]
To assess the anti-inflammatory effects of different fractions of PRF, we exposed murine ST2, 3T3-L1, and calvaria cells along with human gingival fibroblast and HSC2 cells to TNFα and IL1β, either with or without 10% of PPP, BC, albumin gel (Alb-gel), red clot layer (RC), and 30%
Summary
Chronic inflammatory diseases share a conserved pathological mechanism where the immune response fails to remove the detrimental agents, and the resolution of inflammation is hampered [1,2,3]. Chronic inflammation drives a catabolic process that culminates in tissue destruction [4,5] This catabolic process is not restricted to the periodontium, and when not resolved, follows a similar mechanism of destruction as found in rheumatoid arthritis [6], Crohn’s disease [7], psoriasis [8], and refractory leg ulcers [9]. The pro-inflammatory cytokines initiate a feed-forward process whereby neighboring cells are forced to produce pro-inflammatory cytokines and chemokines. These neighboring cells can be of the mesenchymal lineage, including fibroblasts of the soft connective tissue [11]
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