Endotoxin is the lipopolysaccharide component of the cell wall released by gram-negative bacilli when they grow or break down when they die. In vitro and in vivo experiments have proved that endotoxin has the characteristics of heat resistance, acid, and alkali resistance. After endotoxin enters the body, it can cause fever, vasodilation, an increase in vascular permeability, an increase of neutrophils, complement activation, a decrease in blood pressure, and other pathophysiological reactions. In severe cases, it can lead to disseminated intravascular coagulation and multiple organ failure. With the development of basic research and clinical research, people have a better understanding of the structure, function, and mechanism of action of endotoxin. It is also found that the occurrence and development of many diseases are closely related to endotoxin. Endotoxemia may involve surgery, internal medicine, gynecology and obstetrics, pediatrics, neurology, emergency department, etc., but it is still closely related to sepsis, multiple organ failure, acute respiratory distress syndrome, disseminated intravascular coagulation, liver disease, etc. Therefore, it is of great significance to actively carry out basic and clinical research on endotoxin for clarifying the pathogenesis of these diseases and establishing corresponding treatment measures.

Although the research on endotoxin has been carried out for decades, there is still no complete book in China that specifically describes the relationship between the basis of endotoxin and clinical practice. In recent years, with the deepening understanding of the mechanism of action and signal transduction pathway of endotoxin, various strategies for anti-endotoxemia have been established and developed, which provides new ideas for the treatment of endotoxemia in the future.

After endotoxin enters the body, it can directly produce toxicity on the biological membrane of cells, but more importantly, it can make the body produce a variety of inflammatory mediators through the cytotoxic effect mediated by monocyte and macrophage, thus affecting the metabolism of cells, finally leading to cell death, and affecting the integrity of organ function and barrier function. The elucidation of the Toll-like receptor family makes the signal transduction pathway of endotoxin more perfect. It is generally believed that after endotoxin enters the body, it combines with lipopolysaccharide-binding protein to form a complex that transmits lipopolysaccharide to the CD14 receptor on the mononuclear-macrophage membrane, and physical contacts with the domain of toll-like receptor 4 with leucine-rich repeats, which changes the conformation of toll-like receptor 4, Through its cytoplasmic domain, it can recruit intramedullary differentiation protein 88 (My88) and interleukin-1 (IL-1) receptor-associated kinase to undergo self-phosphorylation, trigger enzyme cascade reaction, and finally activate NF-M κ B and other transcription factors, synthesis and secretion of a large number of cytokines play a role.

Many inflammatory mediators are involved in the biological effects of endotoxin, such as TNF- α， Interleukins, NO, complement, prostaglandins, platelet-activating factors, etc. Intestinal bacteria and endotoxin translocation are one of the main factors of endotoxemia, and also an important cause of death of multiple organ failure and liver disease endotoxemias. Emphasis on the treatment of intestinal bacteria and endotoxin translocation is an important means to reduce the occurrence of multiple organ failure in surgical operations and other critical patients and reduce the mortality of patients with liver diseases.

Up to now, there are no specific measures for the treatment of endotoxemia. Although the use of antibiotics can effectively control a bacterial infection, it may increase the risk of endotoxemia. Endotoxin antibody was once considered to be effective in the treatment of endotoxemia, but clinical research has proved that it is ineffective; Other measures include inhibiting lipid A synthesis and blocking endotoxin signal transduction to reduce cytokine secretion, which may be effective in the treatment of endotoxemia, but still need to be confirmed by clinical practice.