Macrophages, thanks to their extreme plasticity, exert critical roles in wound healing by orchestrating tissue defenses in the early inflammatory phase, and by promoting tissue regeneration and angiogenesis at a later time point. In parallel, platelets release a large number of preformed molecules that could affect immunocyte functions. Platelet-rich plasma and platelet lysate (PL) have been widely used as a therapeutic preside for ulcers, although little is known about the effects of platelet-derived biomolecules on macrophage functions during wound healing. In this study, we analyze the effects of PL on macrophages phenotype and functions. Monocyte-derived macrophages were cultured in the presence of interferon-γ and lipopolysaccharides to induce the M1 polarization and were further exposed to 10% PL. PL treatment reduced CD80, CD86, and PDL-1 and enhanced CD206 and CD200R expression on macrophages analyzed by cytofluorimetry. Additionally, macrophage cultures show reduced TNF-α and CXCL10, while increased arginase protein, PPAR, TGF-β, and VEGF. TGF-β secretion was paralleled by the decrease of NFkB and increase of STAT3, STAT6, and SMAD2 and SMAD4. Supernatants of PL-treated macrophages induced a significant increase of type-I collagen and to a lesser extent of type-III collagen production by fibroblasts. Finally, the supernatant of PL-treated macrophages showed significantly reduced capacity to induce the in vitro migration of T lymphocytes. Our results demonstrate that PL dampens the macrophage secretion of pro-inflammatory cytokines and induces the release of arginase, TGF-β, and VEGF that may affect angiogenesis and tissue regeneration, thus facilitating the wound healing process.
Keywords: TGF-β; fibroblasts; macrophages; platelet lysate; wound healing.
© 2021 John Wiley & Sons Ltd.