Gut dysbiosis is characterized by bacteria overgrowth that ultimately leads to increased intestinal barrier permeability and bacteria or bacteria product translocation such as lipopolysaccharide (LPS) in the portal and eventually systemic circulation. Intestinal epithelial cells and hepatocytes encompass enzymatic armamentarium to counteract the LPS toxic effect, however impaired degradation results in LPS accumulation in hepatocytes and endothelial wall. Experimental and clinical study documented that in patients with liver disease, such as non-alcoholic fatty acid liver disease (NAFLD), low-grade endotoxemia by LPS is implicated in liver inflammation and thrombosis via interaction with its Toll-like receptor 4 (TLR4) expressed by hepatocytes and platelets. Furthermore, studies in patients with severe atherosclerosis documented that LPS localizes into atherosclerotic plaque in close association with activated macrophages expressing TLR4 suggesting a role for LPS in vascular inflammation, atherosclerotic progression, and thrombosis. Finally, LPS may directly interact with myocardial cells to induce electric and functional changes leading to atrial fibrillation or heart failure. This review will focus on experimental and clinical evidence suggesting low-grade endotoxemia as mechanism potentially accounting for vascular damage occurring at level of hepatic and systemic circulation and myocardial cells.
Keywords: cardiovascular disease; dysbiosis; endotoxemia; liver; thrombosis.