Disadvantages Of Macrophage

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Macrophages can work in low PH and have a longer lifespan than neutrophil [2]. Macrophage is the key regulator cell that switches the healing process from inflammation to subsequent stages of healing. Macrophage can release anti-inflammatory cytokines such IL10 and TGF-β to promote resolution and healing or release pro-inflammatory mediator such as IL8 to continue acute inflammation by recruiting more neutrophil [9]. Lymphocytes come to the wound site within 72 hours after injury and attracted by IL1, Immunoglobulin G (IgG) product, and complement product. Proliferative phase: At the end of the inflammatory phase, the proliferative phase begins and the proliferation becomes a dominant process. Proliferation is characterized by re-epithelization…show more content…
When the cell become in contact with each other and a new adhesion molecules formed, the migration process stops. Furthermore, the keratinocytes release protein to rebuild the basement membrane. Re-epithelialization process is triggered by many wound associated signals include nitric oxide (NO) which produced by macrophages during early stages of wound healing [16], growth factors including epidermal growth factors (EGF) KGF, IGF-1, and nerve growth factor (NGF) that released from many cell kinds in the wounds. Angiogenesis is a process by which new blood vessel formation is established to supply the damaged area with oxygen and nutrient which are important during wound healing. Angiogenesis is started by by growth factors such as platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and the serine protease thrombin. The remaining endothelial cells of the existing vessels proliferate and migrate toward the angiogenic stimulus. These cells initially form the lumen of the vessels and then differentiate in to venules and arteries and matured by enrolling of smooth…show more content…
Fibroblasts is induced by mechanical tension and cytokines like TGF- to differentiate in to myofibroblasts ,which contract the wound through the expression of smooth muscle actin (SMA). After wound healing process is accomplished, myofibroblasts undergo to apoptosis. During this phase also collagen type I which has high tensile strength replaces type III collagen in the extracellular matrix(ECM). Furthermore, the number of newly formed vessels and blood flow decreased, and mature environment that lack of cells and blood supply is established. Skin appendages like sweat glands and hair follicles can not be retrieved after extreme damage; however, the skin can regain up to 80 % of the original tensile strength

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