1. Red blood cell

As early as the 1950s, people found that if endotoxin was added to sheep red blood cells, they could passively sensitize red blood cells, produce agglutination, and produce complement-mediated cytolysis reaction in the presence of exogenous toxin antibodies. There must be an active substance in the red blood cell membrane that can recognize and bind with endotoxin. Now we know that red blood cells can recognize endotoxin not only through specific recognition (endotoxin receptor), And it can be accomplished by non-specific binding.

Polymyxin B can specifically bind with endotoxin and the active ingredient lipoid A. In the experiment, it was found that in the presence of polymyxin B, many immunologic, immunopathological, and toxic effects of red blood cells dependent on lipid A were inhibited. This strongly suggests that lipid A can combine with some components on the surface of red blood cells, while polymyxin B inhibits this combination, so lipid A cannot mediate its corresponding biological effects.

The nonspecific binding of endotoxin and red blood cells can be achieved not only by passive hydrophobic action but also by active binding.

In a word, there are non-specific and specific binding between endotoxin and red blood cells. The non-specific binding can be carried out by active and passive methods. The endotoxin in the alkaline treatment process increases the non-specific binding and changes some physical and chemical properties of the red blood cell membrane.

2. Platelets

In the presence of plasma protein, endotoxin can affect some functions of platelets. The combination of endotoxin and platelets is the basis of this effect. In most cases, the combination of endotoxin and platelets is completed through the non-specific combination of lipid A and platelet membrane phospholipids. This combination has a relatively low affinity. The reason may be that lipid A is within the endotoxin polysaccharide component and is located in the center of the whole structure, which is difficult to close to the platelet membrane and cannot be fully combined. Similar to red blood cells, lipid A can actively or passively combine with platelet phospholipids, most of which are passive binding, and there is also active binding. It is shown that alkali-treated endotoxin can increase the secretion of platelet granule components and promote the production of platelet factor 3, a phospholipid component of blood coagulation, in a dose-dependent manner. Its mechanism is that alkali-treated endotoxin increases the binding with the platelet membrane and leads to the rearrangement and distribution of phospholipid molecules in the platelet membrane.