Regenerative Inflammation: The Mechanism Explained from the Perspective of Buffy-Coat Protagonism and Macrophage Polarization

Abstract

The buffy-coat, a layer of leukocytes and platelets obtained from peripheral blood centrifugation, plays a crucial role in tissue regeneration and the modulation of inflammatory responses. This article explores the mechanisms of regenerative inflammation, highlighting the critical role of the buffy-coat in influencing macrophage polarization and its therapeutic potential. Macrophage polarization into M1 and M2 subtypes is pivotal in balancing inflammation and tissue repair, with M1 macrophages driving pro-inflammatory responses and M2 macrophages promoting tissue healing and regeneration. The buffy-coat's rich composition of progenitor cells, cytokines, and growth factors-such as interleukin-10, transforming growth factor-β, and monocyte colony-stimulating factor-supports the transition from M1 to M2 macrophages, enhancing tissue repair and the resolution of inflammation. This dynamic interaction between buffy-coat components and macrophages opens new avenues for therapeutic strategies aimed at improving tissue regeneration and managing inflammatory conditions, particularly in musculoskeletal diseases such as osteoarthritis. Furthermore, the use of buffy-coat-derived therapies in conjunction with other regenerative modalities, such as platelet-rich plasma, holds promise for more effective clinical outcomes.

Keywords: buffy-coat; macrophage polarization; mesenchymal stem cells; platelet-rich plasma; regenerative inflammation.

Figure 1

Overview of Platelet-Rich Plasma Preparation. Blood is collected and centrifuged to separate into three layers: red blood cells at the bottom, platelet-rich plasma at the top, and the buffy coat in the middle. This figure shows the approximate cellular composition of the buffy coat, highlighting the distribution of neutrophils, eosinophils, basophils, monocytes, lymphocytes, and platelets.

Figure 2

Macrophage Polarization Pathways. Illustration of signaling pathways involved in macrophage polarization. The NF-κB pathway predominantly supports M1 macrophage activation, promoting pro-inflammatory responses. In contrast, the PI3K/Akt/mTOR and JAK/STAT pathways facilitate M2 polarization, contributing to anti-inflammatory effects and tissue repair. The figure highlights the dynamic interactions between these pathways in response to buffy-coat-derived cytokines and growth factors, which play a pivotal role in the balance between inflammation and regeneration.