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Peripheral Blood Mononuclear Cells

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Pearls and Pitfalls in Skin Ulcer Management

Abstract

Non-healing ulcers considerably impact on patients’ quality of life and place a significant economic burden on healthcare system resources. A whole comprehension of the pathophysiologic cause is crucial in order to establish an effective therapeutic protocol. Non-healing chronic wounds remain blocked in the inflammation phase—the first stage of wound healing. In this stall phase of the repair process, macrophages exhibit an inflammatory phenotype, known as the classically activated M1 macrophage. Over-activated M1 macrophages contribute to the hyperinflammation state by secreting high levels of pro-inflammatory factors and reactive oxygen species (ROS), inducing a premature senescence of resident fibroblasts, thus impairing restoration. The ulcer remains non healing. Induction of anti-inflammatory and regenerative M2 phenotype macrophages at the wound site may facilitate the healing response. Recently, the autologous peripheral blood mononuclear cells (PBMNCs) injection represent a new promising cell therapy used in critical limb ischemia, diabetic foot, and chronic ulcers. PBMNCs show a strong angiogenic capacity combined with the ability to induce the shift from a pro-inflammatory M1 phenotype macrophage to anti-inflammatory, pro-healing M2 phenotype. M2 macrophages are frequently termed “wound healing” macrophages, as they express factors that are essential for tissue repair. It has been demonstrated that autologous PBMNC implants induce M1/M2 phenotype polarization in non-healing wounds, thus inducing tissue regeneration.

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Carella, S., Onesti, M.G. (2023). Peripheral Blood Mononuclear Cells. In: Maruccia, M., Papa, G., Ricci, E., Giudice, G. (eds) Pearls and Pitfalls in Skin Ulcer Management. Springer, Cham. https://doi.org/10.1007/978-3-031-45453-0_26

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