How to affect the LPS synthesis of GNB so that LPS and GNB can be easily recognized and cleared by the host is also a measure to treat endotoxemia. In entheogenic endotoxemia, Escherichia coli (E.coli) has a typical LPS structure, which is easy to escape the host's phagocytosis clearance reaction, shows the strong biological activity of endotoxin, and causes various toxic effects. Therefore, in the study of endotoxins, the LPS of E. coli is often used to evaluate the biological effects of endotoxin and evaluate various intervention measures; When exogenous GNB is infected, its LPS structure lacks the typical LPS structure, and its toxicity is relatively low, which is easy to be cleared by the host.

German scholar Seydel et al. placed LPS aggregate macromolecules in physiological saline, used IL-6 secreted by macrophages as an indicator, and used synchrotron radiation X-ray diffraction technology to analyze the three-dimensional structure of different LPS. It was found that LPS with a cone structure has strong biological toxicity, while the cubic chemical structure of a cylinder structure lacks toxicity or has low toxicity. Hexaacyl lipid A from E.coli is an inverted cube structure, while pentadactyl lipid A and tetradecyl lipid A from E.coli form a multilaminar structure, and tend to have a slight micellar structure; However, c.jejuni lipid A is a unilamellar structure with a slight tendency to develop into an inverted cube structure. All other lipid A forms multilayered structures without exception. Each lipid A of intestinal bacteria hexadecyl is conical or concave, the pentadactyl lipid is mainly cylindrical, and tetradecyl lipid A is cylindrical, and has a tendency to develop to conical or convex (the cross-section of the hydrophobic zone is slightly smaller than that of the hydrophilic zone).

The current data shows that there is a common principle for LPS in endotoxin. Only the conical or concave physical shape of lipid A has high biological activity, such as E. coli in the intestine. LPS lacks agonist activity and is related to the cylindrical shape of lipid A. LPS lacking an acyl group does not mean that it can be used as an antagonist. It may be that when endotoxin is internalized into monocytes, macrophages, neutrophils, and dendritic cells, it is enzymatically hydrolyzed by acyl carboxyl hydrolase (AOAH) to produce deacyl lipid A, and at the same time it changes its three-dimensional morphology. At this time, it has no toxic effect. It can be seen that the presence or absence of acyl groups in LPS does not mean that it is non-toxic. It is necessary to understand its three-dimensional structure.

The biological effect of endotoxin and the amount of negative charge of LPS, the number of acyl chains, the distribution of acyl group, the degree of fatty acid saturation of acyl chain, and the change of stereo conformation all affect the activity of endotoxin. This conclusion can create a theoretical basis for the design of LPS analogs and make them antagonize the effect of toxic LPS.