This research demonstrates how platelet-rich and poor plasma influence inflammation and epithelial response in autoimmune disease through macrophages.
Extracellular traps (ETs) are immune-derived chromatin networks initially described as antimicrobial barriers but increasingly recognized as modulators of tissue homeostasis and autoimmunity. The oral mucosa, constantly exposed to inflammatory stimuli, is particularly sensitive to ET-mediated remodeling (extracellular traps-mediated remodeling). In this study, we investigated how platelet-rich plasma (PRP), platelet-poor plasma (PPP), and washed platelets (WPT), widely used in regenerative medicine, influence ETosis in monocytes and macrophages, and how these ETs modulate the responses of primary buccal keratinocytes (pBMKs). ETs were induced in monocytes/macrophages using PRP, PPP, and WPT. pBMKs were exposed to ET-rich supernatants, and proliferation was monitored in real time through a live cell imaging system. ETs derived from PRP, PPP, and WPT did not induce either a statistically significant proliferation or morphological changes in buccal keratinocytes. These findings suggest that both platelet-derived products (PRP, PPP, WPT) and ETs play a crucial role in modulating epithelial biology, thus suggesting their possible role in chronic autoimmune diseases characterized by persistent inflammation and epithelial remodeling.
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Tonello et al. (2026) studied this question.
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