Impact of inflammatory skin conditions on the biological profile of plasma rich in growth factor

Plasma rich in growth factors (PRGF) can be used over patients suffering from dermatoses due to its anti-inflammatory effect. However, this population group might present soluble autoimmune components and there is limited information about the effect of chronic skin inflammation on PRGF bioactive properties. With the aim of characterizing PRGF composition, PRGF from healthy (H) donors and patients with atopic dermatitis (AD), psoriasis (PS), or lichen sclerosus (LS) was obtained. In order to reduce the inflammatory component, leukocyte exclusion and heat-inactivation (Immunosafe) were tested. Haematological-serological parameters, platelet functionality, clot microstructure, protein content and bioactivity were determined. Mean values and 95 % confidence intervals (mean[95 % CI]) were computed for key haematological parameters, such as platelet (410×10³/mm³[371–449]) and leukocyte content (205×10³/mm³[148−262]), platelet activation (resting: 4.3 %[3.1–5.5] and activated: 97.4 %[96.7–98.0]), the concentration of plasma proteins and morphogens, including immunoglobulins A (210.7 mg/dL[191.8–229.6]), G (933.1 mg/dL[887.2–978.9]), E (783.5 mg/dL[54.4–1512.6]), and M (115.0 mg/dL[97.1–133.0]), Complement Protein (31.6 mg/mL[26.6–36.6]), C-Reactive protein (3.1 mg/L[2.0–4.1]), TGF-β1 (35975.6 pg/mL[34221.3–37729.8]), fibronectin (146410.0 ng/mL[136518.3–156301.7]), PDGF-AB (13308.5 pg/mL[12401.0–14216.0]), CD40L (2389.3 pg/mL[1887.7–2890.8]), IL-4 (0.12 pg/mL[0.07–0.18]), IL-13 (35.4 pg/mL[21.0–49.7]), IL-1β (0.09 pg/mL[0.06–0.11]) and TNF-α (0.31 pg/mL[0.24–0.38]), and also for cell proliferation (332.9ngDNA/mL[317.4–348.3]), viability (135.6 %[132.0–139.2]) and migration (103.8cells/mm²[98.3–109.3]). Plasma from AD donors presented increased Immunoglobulin E (IgE) that was significantly reduced after Immunosafe along with the complement system and autoantibodies. Platelet functionality was altered for AD, but no microstructure differences were identified. Pathological groups presented reduced concentration of fibronectin (AD/LS) and Platelet-Derived Growth Factor (PDGF-AB) (P). Immunosafe treatment reduced Cluster of Differentiation 40 Protein (CD40L), interleukin 1β (IL-1β), and Tumor Necrosis Factor α (TNF-α) concentrations. Fibroblasts supplemented with PRGF obtained from pathological patients (PS/AD) showed reduced viability but Immunosafe increased cell proliferation and migration in SP (LS) and L-SP samples (PS/AD). In conclusion, PRGF derived from pathological patients present autoimmune components, but heat-inactivation or leukocyte exclusion could minimize local side effects.