Inflammatory bowel diseases pathogenesis reflects an integrated activation of signaling events within and between components of the intestine including the epithelial cells, nervous system, immune cells, endothelial cells, and the extracellular matrix [16]. All intestinal resident cells are involved in IBD [12]. Many reports have demonstrated damage to the intestinal microvasculature, epithelial barrier dysfunction, autonomic nerve fiber destruction, as well as myofibroblastic transformation of smooth muscle cells, providing solid evidence for the physical and functional involvement of non immune cells in IBD pathogenesis [18-21]. The enormous complexity of IBD pathophysiology requires a systematic approach to identify the molecular events that cause and sustain inflammation. During my three years of PhD I have focused my attention mainly on the role of two types of non immune cells in the IBD pathogenesis: epithelial cells and endothelial cells. Therefore the objectives of my thesis can be summarized in two principal aims: 1. The involvement of intestinal epithelial cells in the IBD pathogenesis 2. The involvement of intestinal endothelial cells in the IBD pathogenesis.