In£ammatory bowel diseases (IBD) are characterized
clinically by chronic in£ammation in the intestine. The
etiology of IBD remains unclear, even if human and experimental studies indicate that genetic host susceptibility,
gut mucosal immune response and enteric bacteria may
contribute to the pathogenesis of IBD [1]. The importance
of bacteria in sustaining in£ammation in IBD is further
supported by the clinical experience that antibiotics reduce
disease activity. Evidence exists that in patients with active
IBD there is a breakdown of normal tolerance to the resident enteric bacteria £ora which leads to an excessiv