Lipopolysaccharide is composed of hydrophobic lipid A, core polysaccharide, and O-specific polysaccharide (O-antigen) . The lipid A part represents part of the conserved molecular model of LPS and handles most of the biological responses induced by LPS, such as pro-inflammatory responses and septic syndrome . O antigen helps bacteria evade innate immune responses, including phagocytosis and complement-mediated lysis . Lipopolysaccharide activates the natural immune system response in the adipose tissue of patients with obesity and type 2 diabetes and increases the risk of endotoxinism and disease . Patients with type 2 diabetes have significantly increased LPS levels and LPS activity. It positively correlated LPS with inflammation markers and poor blood glucose/lipid control . Late complications (such as massive albuminuria) exacerbate endotoxemia. Clinical reports have shown that the level of LPS in the plasma of patients with severe COVID-19 is increased, and the level of endotoxin is significantly increased . Lipopolysaccharides (LPS) in the blood also induce reactions by interacting with lipopolysaccharide-binding protein (LBP) in the serum . LBP levels of obesity are also high . It closely related serum LBP levels to the hospitalization rate of COVID-19 patients . LBP's plasma levels in hospitalized COVID-19 patients with obvious cardiology are initially high and remain high during hospitalization . It shows that SARS-CoV-2 infection causes an increase in endotoxemia of infected individuals. SARS-CoV-2 infection also induces a "leaky gut" state . SARS-CoV-2 RNA is found in stool samples of hospitalized COVID-19 patients, and it reported diarrhea symptoms . Therefore, the intestinal state caused by endotoxemia is a chronic sequelae of COVID-19.