Review the mechanisms by which endothelial cells contribute to inflammation in key diseasesThe endothelium is a cell layer that is lined on the inner surface of lymphatic vessels and blood vessels, which are made up from endothelial cells (Dorland, 2012). Endothelial cells in direct contact with blood cells are called vascular endothelial cells while those in contact with lymph are called lymphatic endothelial cells. In addition to regulating hemostasis, endothelial cells also possess important functions such as permeability, regulation of vascular tone, immunity, leukocyte trafficking, inflammation, and angiogenesis, among others.[1] [2] [3]. Inflammation is the body's tissue reaction to injury, fundamental in the innate and adaptive response. The signs of inflammation are characterized by rubor, dolor, tumor and calor, i.e. redness, pain, swelling and heat respectively. The benefits of inflammation outweigh the adverse effects and is important for survival, although excessive inflammation could cause harm, such as sepsis or septic shock[4]. The inflammation process to which endothelial cells contribute begins with endothelial hyperpermeability when mediated by inflammatory agonists. The increased permeability allows transendothelial migration of cells such as leukocytes. The whole process begins when an involved agonist binds to receptors specific to it, expressed on the surface of endothelial cells, activating enzymes such as phospholipase C (PLC) directly through vascular endothelial growth factor receptors (VEGFR) or by thrombin or histamine through G protein-coupled receptors (GPCRs). Once binding has occurred, a cascade of signals will begin the reactions, with Rho guanosine-5'-triphosphate (Rho GTPase) as the rho-ace...... at the center of the paper ......n of the valves. ClfA mediates adhesion to nonbacterial thrombotic endocarditis (NBTE) followed by FnbpA causing endothelial cell internalization, inflammatory and coagulation responses[12]. Fibronectin, which is a ligand for bacteria expressing fibronectin-binding proteins, binds to integrins, expressed by inflamed endothelial cells, causing increased susceptibility to adhesion, tissue necrosis, inflammation, and vegetation growth. In conclusion, Endothelial cells in atherosclerosis cause increased expression of surface adhesion molecules which results in an increase in the amount of leukocytes attracted to the site and therefore causing more inflammation than usual. In infective endocarditis, NBTE allows bacterial adhesion of the heart valves, mediated by ClfA and then FnbpA. This causes a series of reactions ranging from vegetative growth to inflammation.