• colitis
• signal transduction
• T lymphocytes
• fibre
• transcription
• Cdx2 homeobox gene
• butyrate
• colon cancer

Ulcerative colitis (UC) and Crohn's disease (CD), the most predominant manifestations of inflammatory bowel diseases (IBD), are accelerating major health problems. Although the aetiology of IBD remains elusive, a great deal of work has been carried out in successfully identifying some of the pathological and clinical profiles that are perturbed in these patients. This has led to the description of some of the molecular mechanisms that may underlie the idiopathic inflammation encountered in IBD. More recently, gene families and clusters which may be implicated in the onset of IBD, albeit in a limited manner, have been discovered.

Cytokines such as interleukin (IL)-1, IL-6, tumour necrosis factor α (TNF-α), and interferon γ among others, have been shown to maintain the highly chronic inflamed state of the bowel, if not actually causing the onset of this condition. Hence one (major) effort to uncouple the vicious circle and to combat this disease has been to eliminate or diminish the effects of these cytokines. The use of molecules blocking cytokine receptor interactions, by disrupting the means of cytokine activity (for example, inhibiting nuclear factor κB …