The two major forms of human inflammatory bowel disease (IBD), Crohn’s disease (CD) and ulcerative colitis (UC), represent classic chronic inflammatory disorders, characterized by progressive destructive inflammation in the gastrointestinal tract. Although the majority of research into IBD pathogenesis has focused on immune dysregulation, vascular involvement in IBD has also been recognized over the past four decades, as these disorders have been associated with hypercoagulability and vasculitis. Advances in vascular biology have delineated a central role for the microcirculation in the initiation and perpetuation of the inflammatory process. Investigation in the molecular and cellular mechanisms underlying human IBD has demonstrated an important role for the intestinal microvascular endothelium in both mucosal immunity as well as the chronic inflammation that characterizes IBD. Chronically inflamed microvessels and endothelial cells in the setting of IBD show significant alterations in physiology and function compared with microvessels and cells from uninvolved the intestine, where IBD microvessels demonstrate an enhanced capacity to adhere leukocytes. Understanding of leukocyte-endothelial interaction in IBD is presently leading to new antiadhesion molecule agents that target the vasculature for therapy.
Hatoum OA, Miura H, Binion DG. The vascular contribution in the pathogenesis of inflammatory bowel disease. Am J Physiol Heart Circ Physiol. 2003;285(5):H1791-H1796. doi:10.1152/ajpheart.00552.2003