Inflammatory Bowel Disease (IBD) is a chronic, relapsing, immunologically-mediated disorder of the intestine that contains two major forms of disease: Ulcerative Colitis and Crohn’s Disease.   Both are characterized by the presence of intestinal inflammation and diarrhea.  Ulcerative colitis is an inflammatory disease of the large intestine (colon) with inflammation typically limited to the mucosal surface.  Crohn’s Disease, on the other hand, may involve the entire gastrointestinal tract from the mouth to the anus, although the terminal ileum and the right colon are most commonly affected.  In Crohn’s Disease the inflammation is not limited to the mucosal surface, but involves the entire bowel wall.

IBD is categorized based on clinical manifestations and has been studied for decades; yet the underlying pathophysiologic processes are not completely understood.  The prevailing theory is that IBD is the result of an abnormal immune response to environmental triggers in a genetically susceptible host.  Although not considered an autoimmune disease per se, IBD shares in common with autoimmune diseases such as Celiac Disease and Type 1 Diabetes, the following characteristics that appear to contribute to development of disease:

• Genetic factors
• Defects in barrier function of the intestinal epithelium
• Environmental factors
• An aberrant immune response

IBD is largely a disease of the twentieth century and is associated with the rise of modern, Westernized industrial society.  Both Ulcerative Colitis and Crohn’s disease are common in North America and becoming more common in other countries as they adopt a Western lifestyle.  As many as 1.4 million people in the US and 2.2 million in Europe suffer from these diseases.  The incidence of Crohn’s Disease appears to be increasing, while that for ulcerative colitis is stable.  The mean age at diagnosis for Crohn’s Disease is mid-30s to early 40s while the mean age at onset of ulcerative colitis can be somewhat younger, particularly among men.  Both Ulcerative Colitis and Crohn’s Disease, however, can occur in younger adults, adolescents, and children.

Many studies have demonstrated altered tight junction structure and consequent epithelial barrier defect in both Ulcerative Colitis and Crohn’s Disease.  Defective barrier function, which can be measured as increased intestinal permeability, can predict relapse during clinical remission of patients with Crohn’s Disease and disease suppression with anti-TNF antibodies restores barrier function.   These observations support the concept that in IBD, increased intestinal permeability allows overexposure to environmental antigens which in turn initiate and maintain inflammation of the bowel wall.   Alba’s therapeutic approach includes regulation of intestinal tight junctions to prevent the overexposure of antigens and the consequential inflammatory cascade clinically presented in Crohn’s patients.