Vascular endothelial cells (ECs) perform a number of functions required to maintain homeostasis. Inflammation can cause EC injury and death which disrupt these processes and result in endothelial dysfunction. Three common mediators of EC injury in inflammation are macrophage-derived cytokines, such as tumour necrosis factor (TNF); neutrophil-generated reactive oxygen species (ROS) and cytolytic T lymphocytes (CTL). Here we describe the distinct but overlapping biochemical pathways of injury elicited by these different agents.