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. 2018 Jul 1;7(7):209–231. doi: 10.1089/wound.2017.0761

Figure 3.

Figure 3.

Overview of the immune mechanisms in acute and chronic wound healing. (A) Acute wound healing results from a well-coordinated series of events divided into four overlapping phases: hemostasis, inflammation, proliferation/matrix deposition, and tissue remodeling. Neutrophils and macrophages are particularly important in mediating this process, though T cells and platelets also play key roles. (B) High numbers of inflammatory cells and the formation of a biofilm preclude the restoration of tissue homeostasis in chronic wounds. Excess secretion of inflammatory mediators leads to growth factor and ECM degradation and prevents macrophage phenotype conversion, which creates a feed-forward loop preventing resolution. Black arrows indicate differentiation, blue arrows indicate inhibition and red arrows indicate induction. CXCL, C-X-C chemokine ligand; ECM, extracellular matrix; FGF, fibroblast growth factor; IL, interleukin; MMP, matrix metalloproteinase; NET, neutrophil extracellular trap; ROS, reactive oxygen species; TGF, transforming growth factor; TIMP, tissue inhibitor of matrix metalloproteinase; TNF, tumor necrosis factor.

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