During sepsis, however, blood-borne proinflammatory mediators are released, coincidental with diffuse endothelial activation and subsequent upregulation of vascular adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1), E-selectin on cerebral endothelia [42-45], facilitating adhesion and transmigration of neutrophils and monocytes into the brain tissue. Here, ICAM1 is linked to Sepsis.