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• W152474198 abstract "The inflammatory bowel diseases (IBD; Crohn’s disease, ulcerative colitis) are chronic, idiopathic inflammatory disorders of the intestine and/or colon characterized by rectal bleeding, severe diarrhea, abdominal pain, fever and weight loss. Histologic examination of biopsies obtained from patients with active episodes of IBD reveal the infiltration of large numbers of leukocytes such as polymorphonuclear leukocytes (PMNs), monocytes, and lymphocytes into the intestinal interstitium. Extensive mucosal and/or transmural injury and dysfunction including edema, loss of goblet cells, decreased mucous production, crypt cell hyperplasia, erosions and ulcerations, accompany this inflammatory infiltrate. Despite several years of intense investigation, the etiology and specific pathogenetic mechanisms responsible for IBD remain poorly defined. Recent experimental and clinical studies suggest that the initiation and pathogenesis of these diseases are multi-factorial involving interactions among genetic, environmental and immune factors [1]. Regardless of exactly how these interactions ultimately promote chronic gut inflammation, it is becoming increasingly apparent that the immune system plays a crucial role in disease pathogenesis. Because the inflammation is localized primarily to the intestinal tract in IBD, investigators have focused on the intestinal lumen as the site for the antigenic trigger. Indeed, the chronic relapsing nature of IBD coupled to the fact that a large percentage of patients with Crohn’s disease will experience recurrence of the disease following surgical resection of the bowel, suggests that the antigen or antigens that initiate and perpetuate this disease are part of the normal gut flora. Different etio-logic theories have been proposed to account for this apparent mucosal immune system activation, however, data obtained from numerous experimental studies suggest that chronic gut inflammation may result from a dysregulated immune response to components of the normal gut flora [2]. For example, several groups of investigators have shown that targeted deletion of certain genes known to be important in regulating the inflammatory response or immune manipulation in mice induces chronic colitis in these animals [3]. Furthermore, the colonic inflammation observed in virtually all of these animal models is dependent upon the presence of normal gut flora. Animals raised under germ-free conditions either fail to develop disease or develop much milder forms of colitis [3]. These studies have lead investigators to suggest that bacterial/immune interactions in individuals with defects in their immune system may represent an important pathophysiological mechanism for the development of IBD in humans." @default.
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• W152474198 date "2001-01-01" @default.
• W152474198 modified "2023-10-12" @default.
• W152474198 title "Role of nitric oxide in chronic gut inflammation" @default.
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• W152474198 doi "https://doi.org/10.1007/978-3-0348-8241-5_10" @default.
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