Abstract
IBD include two major pathologies, ulcerative colitis (UC) and Crohns Disease (CD), both characterized by an exaggerated response of the mucosal immune system to stimuli originated from the intestinal flora. Alterations in intestinal permeability and regional and systemic immune responses may play a role in disease outcome. In UC and CD release of Tumor Necrosis Factor (TNF)-α has been invoked as one of the major factor in the chronicity of the inflammation and this sustained production of TNF-α can be supported by plasma endotoxins detectable in a large percentage of IBD patients. In this framework, the role of enteric bacteria in the pathogenesis of IBD is discussed. The availability of Infliximab, a chimeric monoclonal antibody (MoAb) against TNF-α, has represented a therapeutical advance in the treatment of CD patients. In CD patients with moderately active disease, a single infusion of Infliximab led to a significant reduction in their score on a standard CD activity index and one third of the total achieved actual clinical remission. However, the response lasted from a few weeks to six months or more. Same pattern of responsiveness was seen in patients with perianal and cutaneous fistulas. According to some completed trials, serial administration of the drug seems to be more efficacious to maintain the initial response., however this indication has not yet been approved. The mechanisms of action of Infliximab are, then, described and personal data with a cytofluorimetric method for the immune follow-up of CD patients under Infliximab treatment are reported. Finally, among the side effects of Infliximab, cases of active tuberculosis have been described after the initial treatment.
Keywords: tumor necrosis factor, inflammatory bowel disease, cytokines, bacteria
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