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The cause of death for burn patient, especially the severe burns, is complicated. During the whole process of burn there are many harmful matters released from the necrosis tissues and producted from the secondary inflammation reaction, which can decrease the defense function and easily lead to inflammation , the failure of internal organs and finally death. The uncontrolled inflammation reaction is commonly called“mediator disease”. After burn, numerous promoting inflammation cytokines, which is the clues of uncontrolled inflammation reaction and the products of cascade inflammation reaction, is one of the causes to the cells and tissues injury. As a result, in order to augment the cure rate of severe burns, the cytokines released from wound surface at early stage are the focus.Interleukin 8 is a muti-source cytokine, coming from monocyte, macrophage, fibroblast , T cell , osteosarcoma cells and so on, especially monocyte and macrophage. After burn, especially the severe burn, interleukins 8 in wound blister, wound secrets and plasma is increased significantly. The transcription of its mRNA is enhanced. The high concentration of interleukins 8 in wound could promote the infiltration of neutrophilic granulocyte, extend the area of necrosis wound, destroy the remained skin appendage, decelerate the heal of wound and lead to systemic inflammation after burns. Persistent increase of interleukin 8 may associated with serious Multiple organ dysfunction syndrome and toxemia.Macrophage(MΦ) is an important cells, which could be activated to be an effective inflammation cells with phagocytosis and secretory function to release complements, blood coagulation factors, activity enzymes, hormones and cytokines such as interleukin 1, interleukin 3, interleukin 6, interleukin 8, TNF, IFN, FCF and so on. In vitro, a simple signal pathway of cascade inflammation reaction, necrosis tissue→interleukin 8→macrophages→interleukin 1, interleukin 6 and TNF→systemic inflammatory response syndrome and SIRS, have been proved. Therefore, there may be a
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