LBP (lipopolysaccharide binding protein) is mainly synthesized and secreted by hepatocytes. The LBP gene in human hepatocytes is located between q11, 23, and q12 in the long arm of chromosome 20; The LBP gene of humans and rabbits has been cloned and its nucleotide sequence has been clarified.

IL-6 is a necessary condition for LBP synthesis. IL-6 can activate relevant transcription factors through signal transduction and promote the transcription of the LBP gene and the synthesis and secretion of LBP in human hepatocytes. In the absence of IL-6, the amount of LBP synthesized by hepatocytes cultured in vitro is very small, and the amount of LBP synthesis will be further reduced after 39 hours; After adding IL-6, the synthesis amount of LBP increased significantly and did not decrease with time. Use IL-1 and TNF separately- α Neither L-6 nor dexamethasone can promote LBP synthesis, but they can enhance the effect of IL-6 on LBP synthesis, especially in the presence of L-6 and dexamethasone, or IL-6 and TNF- α At the same time, LBP synthesis can be significantly enhanced by stimulation.

Human hepatocellular carcinoma cell line Hep G2 can synthesize and secrete LBP. Hep G2 cells are immortal cells, which can be subcultured in vitro for a long time. They are often used to study the synthesis of LBP and its influencing factors.

Robert et al. have cloned the LBP gene fragment (cDNA) from human liver cells using the EB virus as a vector and integrated it into the DNA of the human kidney cell line (293-EBNA cell line) to produce recombinant human LBP for the first time.

LBP is synthesized by hepatocytes and secreted into the blood, which is present in normal human and animal serum. In the human body, the normal value of LBP is 3~7mg/L, and its value rises 50~100 times during inflammation.

LBP belongs to the acute phase response protein. In the stress state, if the body's blood encounters a small number of endotoxins for 6 to 12 hours, the synthesis and secretion of LBP by the liver will increase significantly, and the amount of LBP released is proportional to the amount of endotoxin in the body and the duration of its existence. Patrick et al. believed that plasma LBP level could be used as a marker for the diagnosis and prognosis of sepsis and corresponding endotoxemia. White et al. reported that the level of LBP in infectious diseases was significantly higher than that in healthy people and patients with noninfectious diseases. The continuous peak or continuous rise of LBP is significantly related to the case fatality rate.

LBP, together with bactericidal/osmotic enhancer protein, cholesterol ester transfer protein, and phospholipid transfer protein, forms a homologous lipid-binding protein family. In the absence of LBP, the binding speed of LPS and CD14 molecular cells decreased by less than 1000 times compared with that in the presence of LBP. High concentrations of LPS can also directly act on megakaryocytes, but LBP plays an important role in promoting the LPS-induced production of inflammatory mediators in megakaryocytes. Therefore, the combination of LBP and LPS can significantly increase the phagocytosis of megakaryocytes to bacteria and promote TNF- α The role of secretion.