MEDIATORS OF INFLAMMATION - PRODUCTION AND IMPLICATION IN INFLAMMATORY BOWEL-DISEASE

Ulcerative colitis and Crohn's disease, regardless of the initiating e vents, share common immunologically mediated pathways of tissue injury and repair. Although; their etiology remains unknown, increasing evid ence suggests that activated immunological effector mechanisms within the intestinal mucosa are responsible for the pathogenesis of the dise ases. Activation of immune, mesenchymal and epithelial cells; transmig ration 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 respons e, synthesis and release of enzymes, and cell proliferation. In the la st decades, the identification of potential mediators in intestinal in flammation has expanded to include eicosanoids, platelet activating fa ctor, biogenic amines, kinins, proteases, reactive oxygen species, com plement components, cytokines, chemokines, nitric oxide, and neuropept ides. An increasing understanding suggests that in inflammatory bowel disease, regardless of the predisposing and trigger factors, a disrupt ion of certain regulatory mechanisms, mediated by these soluble molecu les, results in pathological immune responses to antigens and in chron ic inflammation.