Gene Ontology Analysis for Drug Targets of the Whole Genome Transcriptome of Human Vascular Endothelial Cells in Response to Proinflammatory IL-1

Abstract

The innate immune system combats tissue injury and infection by activating the proinflammatory responses involving the humoral complement system, granulocytes, macrophages and vascular endothelial cells (VEC) (Newton and Dixit, 2012; Zhu et al., 2012). Macrophages mediate proinflammatory responses by releasing inflammatory cytokines such as IL-1β. Once secreted, IL-1β paracrinically acts on the VEC and massively change their functions. These perturbations include a change from the anticoagulant phenotype to a procoagulant state, enhanced expression of vasoactive substances, cell adhesion molecules as well as inflammatory mediators including chemoattractants, and endothelial barrier dysfunction causing microvascular leakage (Pober and Sessa, 2007). Although essential for the effective immune defense, uncontrolled or chronic inflammatory response causes tissue damage and loss of organ function (Lon et al., 2012).