Acute respiratory distress syndrome (ARDS) is a distinct type of hypoxic respiratory failure characterized by acute bilateral lung abnormalities. The pathophysiology of ARDS is complex, involving the activation and dysregulation of multiple overlapping and interacting pathways of pulmonary and systemic injury, inflammation, and coagulation. Endotoxins are lipopolysaccharides (LPS) in Gram-negative bacteria that have very high pro-inflammatory properties. Endotoxin in the circulating blood stimulates the monocyte-macrophage system to produce inflammatory factors such as tumor necrosis factor, interleukin-1, and interleukin-6, which stimulates the inflammatory cascade effect and aggravates the original clinical symptoms. Exposure to high concentrations of endotoxin induces systemic and airway inflammatory disease, causing severe trauma to the lungs. Current studies have confirmed that endotoxin is one of the main factors leading to occupational lung diseases, so the detection of endotoxin levels in patients may become a powerful tool in the diagnosis of lung injury in clinical applications.
Figure 1. Amelioration of LPS-induced alveolar inflammation by nimbolide. (Pooladanda V, et al., 2019)
ARDS is a clinical syndrome associated with respiratory dysfunction, the complications of which are usually septicemia and sepsis, leading to clinical manifestations of chest tightness, shortness of breath, and intermittent dyspnea. Endotoxin is a bioactive component of the cell wall of Gram-negative bacteria and exists as a complex of lipopolysaccharide and protein. During sepsis or bacterial pneumonia, endotoxins released from Gram-negative bacteria can cause severe lung injury. Both conditions are predisposing factors for ARDS, so endotoxins can be used in animal models of lung injury in several related conditions. The current pilot study has demonstrated that intraperitoneal administration of certain amounts of endotoxin to mice used as a model of lung inflammation results in transient lung injury and dysfunction. In addition, endotoxin has a significant impact on the function of the airway and pulmonary circulation and then causes a series of respiratory diseases in the whole animal model. At present, clinical examinations for ARDS are mainly through the measurement of partial pressure of oxygen, chest X-ray, and CT. As a result, multiple examinations are needed to assist differential diagnosis, which is time-consuming and prone to misdiagnosis. By detecting the endotoxin level in the patient's body fluid, it is more convenient and quicker to help medical staff determine the condition of lung injury, and further accurately judge the disease.
The results of past experiments have shown that if endotoxin is injected into the lungs, it will cause a series of chemokines, inflammatory factors, and cytokines to malfunction, resulting in severe inflammatory reactions. At the same time, it releases many active media to produce toxic effects on pulmonary capillaries and alveolar tissue, resulting in pulmonary edema, extensive micro thrombosis, and respiratory insufficiency. In vitro and in vivo models of acute lung inflammation have been widely used to elucidate the molecular mechanisms of endotoxin-induced lung injury. Within 1 hour, endotoxin detection can detect the presence of endotoxin in the blood and organs of the human body, determine whether it is infected based on indicators, and help diagnose disease. The detection methods mainly include the dynamic turbidity method, endpoint chromogenic method, endpoint turbidity method, and dynamic chromogenic method, which are beneficial to observe the state of the body. Therefore, endotoxin detection has certain clinical significance for the early lung injury caused by endotoxin, and can effectively prevent and assist in the treatment of lung-related diseases.
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