Ulcerative colitis and Crohn's disease, regardless of the initiating events, share common immunologically mediated pathways of tissue injury and repair. Although their etiology remains unknown, increasing evidence suggests that activated immunological effector mechanisms within the intestinal mucosa are responsible for the pathogenesis of the diseases. Activation of immune, mesenchymal and epithelial cells; transmigration of leukocytes from the circulation to the sites of inflammation; tissue damage; and healing phase are mediated by a number of soluble mediators released by activated intestinal cells. These mediators are involved in a network of cell communication, affecting immune response, synthesis and release of enzymes, and cell proliferation. In the last decades, the identification of potential mediators in intestinal inflammation has expanded to include eicosanoids, platelet activating factor, biogenic amines, kinins, proteases, reactive oxygen species, complement components, cytokines, chemokines, nitric oxide, and neuropeptides. An increasing understanding suggests that in inflammatory bowel disease, regardless of the predisposing and trigger factors, a disruption of certain regulatory mechanisms, mediated by these soluble molecules, results in pathological immune responses to antigens and in chronic inflammation.