Atherosclerosis (AS) is the most common cause of coronary heart disease, cerebral infarction, and peripheral vascular disease, characterized by the accumulation of lipids in the arterial intima and the appearance of yellow atheroma. The symptoms are lipid and complex carbohydrate accumulation, hemorrhage and thrombosis, fibrous tissue hyperplasia, and calcinosis. AS begins in childhood and progresses continuously, with symptoms usually appearing in middle age or older age. Endotoxin is a lipopolysaccharide (LPS), a component of Gram-negative bacterial membranes, that can be translocated into the systemic circulation, resulting in non-septic development. Both endotoxin and its inducers can cause damage to vascular endothelial cells, thereby affecting the occurrence and development of AS. The possible mechanism of the effect is that the endotoxin can directly damage the vascular endothelial cells, or that the endotoxin can cause the increase of the triglyceride content in the plasma. It is also possible that endotoxin and its activating substances can increase the activity of thrombin, which can lead to a decrease in the activity of the body's physiological anticoagulant mechanism, an increase in fibrin, and a coagulation reaction. Through the above three ways, the condition of AS is aggravated and worsened.
Figure 1. Mechanisms of LPS-mediated atherosclerosis. (Violi F, et al., 2023)
Cardiovascular and cerebrovascular diseases, mainly AS, are the diseases with the highest morbidity and mortality. Endotoxin, as a risk factor for AS, has attracted much attention. Endotoxin, also known as lipopolysaccharide (LPS), negatively affects body homeostasis by translocating into the systemic circulation, shifting host immune defenses to a pro-inflammatory state, which has been shown to predispose to AS. The innate immune system recognizes LPS as a pathogen-associated molecular pattern, such as the Toll-like receptors (TLRs) associated with AS and thrombosis. Daily intravenous or intraperitoneal infusion of LPS accelerated aortic atherosclerosis and increased the production of pro-inflammatory cytokines in animal models, further confirming that LPS is a pro-atherogenic molecule. In addition, LPS has also been shown to destabilize atherosclerotic lesions, thereby making atherosclerotic plaques more susceptible to rupture or erosion. At present, the detection of LPS has been used in different clinical applications, including rabbit pyrogen detection, limulus amoeba cell lysate determination, enzyme-linked immunosorbent assay, biosensor, etc. Therefore, the determination of LPS activity or concentration in the patient's blood plays a positive role in the clinical diagnosis of AS.
Environmental endotoxins trigger the intracellular transcription of several inflammatory mediators when they enter the systemic circulation. AS is gradually recognized as a chronic inflammatory disease, and bacterial endotoxin has been identified as a potentially important factor in vascular inflammation in AS. Therefore, the detection of endotoxin in the patient's blood is helpful for the clinical diagnosis of bacterial infectious diseases. The application of the limulus test to detect endotoxin can quickly conclude, especially for patients with endotoxin shock. At the same time, it has a certain auxiliary effect on the prevention and early treatment of AS.
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