Human idiopathic inflammatory bowel disease (IBD), Crohn disease (CD) and ulcerative colitis (UC) are lifelong illnesses characterized by chronic inflammatory destruction of the gastrointestinal tract. IBD is estimated to affect between one to two million Americans, and is most commonly diagnosed during adolescence or early adulthood, thus representing a significant burden of disease throughout the patient's lifetime (1). The description of terminal ileitis in 1932, later commonly referred to as CD, distinguished chronic intestinal inflammation and stricture formation from intestinal tuberculosis (2), in which the resected gut tissues failed to demonstrate acid-fast bacilli on histological examination. The anatomic distribution of CD was later revised to include the large bowel (3, 4). Samuel Wilks initially described UC, distinguishing it from hemorrhagic bacterial dysentery by 1859. The first description of the natural history of UC was reported in 1909. Despite decades of intense research efforts, the etiology of IBD remains obscure and, as a result, treatment options are not specific and focus on blunting the chronic inflammatory process in the gut. A majority of CD patients ultimately require surgical intervention for complications, most commonly the emergence of symptomatic strictures in the intestinal lumen. Approximately one fourth of UC patients require colectomy for the treatment of medically refractory disease or the detection of neoplastic transformation, a well-recognized complication of long-standing chronic gut inflammation. Recent evidence from genetic and immunologic investigation has identified alterations in the innate immune response and inappropriate immune activation of the mucosal immune system in response to enteric microbiologic antigens as a potential inciting influence in the development of IBD.