When laboratory tests are performed on patients suffering from sepsis, the white blood cell count is significantly increased, usually up to (20-30) x 109/L or more, or decreased, left-shifted, or increased naive type, and toxic granules appear. Normally when microorganisms invade the body, the body’s immune defense system responds rapidly and appropriately; however, when the immune defense is defective, over or under responsive, it can lead to the development and progression of sepsis through endogenous inflammatory substances. Early on, the key role is played by cytokines. Under endotoxin stimulation, monocytes produce inflammatory factors such as tumor necrosis factor (TNF) and interleukin-1 (IL-1), which promote neutrophil adhesion to endothelial cells, activate the coagulation system, and release large amounts of inflammatory mediators, including other cytokines, leukotrienes and proteases, as well as anti-inflammatory mediators such as IL-6, IL-10, etc. IL-1 IL-1 and TNF have synergistic effects and have many of the same biological effects. Studies in animal models of sepsis have shown that inhibition of IL-1 and TNF can improve organ function and increase survival, IL-8 can chemotactic neutrophils and lead to prolonged inflammation, IL-6 and IL-10 may play a negative regulatory role, inhibit TNF production, enhance the role of acute chronotropic substances and immunoglobulins, and suppress the function of T lymphocytes and macrophages. However, only one of the many clinical studies suggests that altered concentrations of TNF have physiological effects and can affect cytokine levels downstream of the immune cascade. Arachidonic acid metabolites are associated with the development and progression of sepsis, and animal and clinical trials have observed that cyclooxygenase inhibitors (ibuprofen) can lower body temperature, slow heart rate, reduce ventilation per minute, and correct lactic acidosis by inhibiting the production of these substances, but do not reduce mortality. It was further confirmed that thromboxane A2 (vasoconstrictor), prostacyclin (vasodilator) and prostaglandin E2 are involved in the development of fever, tachycardia, shortness of breath, ventilatory dysfunction, and lactic acidosis. Sepsis is a common complication after severe trauma, burns, shock, and major surgery, and is an important cause of death in critically ill surgical patients. Current studies generally agree that the activation of neutrophil, lymphocyte and mononuclear macrophage systems and their release of endogenous mediators play a key role in the pathophysiological mechanisms of post-traumatic sepsis.