1. Effect on endothelial cells

When endotoxin is injected into the veins of mice, rabbits, dogs, baboons, and other animals, the presence of endotoxin can be found in the endothelial cells of capillaries such as the liver, lung, intestinal wall, spleen, kidney, etc. The endothelial cells have pathological damage changes, nuclear deformation, vacuoles in the nucleus, followed by nuclear disappearance, and even the endothelial cells fall off from the vascular wall and enter the blood circulation. Endotoxin itself activates endothelial cells and promotes the expression of cytokines, NO, oxygen free radicals, chemokines, prostaglandins, etc. These inflammatory factors promote cell damage through autocrine, paracrine, and other ways. After endothelial cell damage and apoptosis, it can expose its vascular basement membrane, activate Hageman factor, activate the coagulation system, and lead to local coagulation or disseminated intravascular coagulation, the endothelial cell gap increases, and vascular permeability increases, Vasoactive substances such as bradykinin are elevated, and the expression of integrin is enhanced. Under the combined action of chemokines and other factors, neutrophils and monocytes are promoted to migrate under the endothelium, resulting in increased damage.

2. Effect on mast cells and basophils

After injecting endotoxin into the abdominal cavity of mice for 5 hours, the number of incomplete mast cells in the abdominal cavity increased significantly. After 18 hours, the number of mast cells decreased by 70%, accompanied by a significant increase in macrophages and an increase in peritoneal permeability. Its mechanism is not clear. Because mast cells are not the main effector cells of endotoxin, and the distribution of various endotoxin receptors is very small, such as CD14, TLR4, etc., the effect on endotoxin is weak. However, after activation of macrophages, and under the secretion of various inflammatory factors, it can act on mast cells. Although the in vitro experiment failed to prove that endotoxin has a direct activation effect on mast cells and basophils, it is not ruled out that mast cells and basophils also participate in the pathogenesis of endotoxic shock, because mast cells can degranulate and release their vasoactive substances to participate in the occurrence of DIC, Shuck, etc.

3. Effect on erythrocyte and serum iron

Endotoxin can inhibit the formation of red blood cells. It may be the precursor cells of red blood cells directly acting on the bone marrow, or it may also inhibit the role of erythropoietin, or other hematopoietic factors, which inhibit the differentiation of hematopoietic stem cells into erythroid. In addition, endotoxin can combine with erythrocyte membrane to form a complex antigen, stimulate B lymphocytes to produce antibodies, and produce a hemolytic reaction with the participation of complement.

In animals, endotoxin can easily reduce serum iron concentration. Wolff et al. injected Salmonella equine abortus into the human body, resulting in a significant reduction in serum iron concentration. The mechanism is unclear. It may be that it can promote the synthesis of globin in a large amount and combine with free iron to reduce serum iron.