Causes:

Researchers do not know the exact causes of inflammatory bowel disease. IBD appears to be due to an interaction of many complex factors including genetics, impaired immune system response, and environmental triggers. The result is an abnormal immune system reaction, which in turn causes an inflammatory response in the bodyâ ' s intestinal regions.

The Inflammatory Response

The Immune System's Infection Fighters. The primary infection-fighting units are two types of white blood cells: lymphocytes and leukocytes.

Lymphocytes include two subtypes known as T cells and B cells. Both types of cells are designed to recognize foreign invaders (antigens) and to launch an offensive or defensive action against them:

• B cells produce antibodies, substances that can either ride along with a B cell or travel on their own to attack the antigen.
• T cells have special receptors attached to their surface that recognize the specific antigen.

T cells are further categorized as killer T cells or helper T cells.

• Killer T cells directly attack antigens that occur in any cells that contain a nucleus.
• Helper T cells also recognize antigens, but their role is two-fold. They stimulate B cells and other white cells to attack the antigen. They also produce cytokines, powerful immune factors that have an important role in the inflammatory process.

Helper T Cells and Inflammatory Bowel Disease. The actions of the helper T cells (TH cells) are of special interest in inflammatory bowel disease:

• TH cells stimulate other white blood cells called B cells to produce antibodies. In this case, however, they appear to direct the B cells to produce autoantibodies, which then turn against the body's own cells.
• TH cells also secrete or stimulate the production of powerful immune factors called cytokines. Cytokines, particularly specific ones known as tumor necrosis factor, interferon-gamma, and interleukins, cause intestinal inflammation and damage, which, in a vicious cycle, attract even more helper T cells.

Helper T cells are further categorized as TH1 and TH2. An imbalance in these two types appears to occur in inflammatory bowel disease (IBD), although each disorder has a different balance.

Genetic Factors

Although the exact causes of inflammatory bowel disease are not yet known, genetic factors certainly play some role. Between 10 - 20% of people with ulcerative colitis have family members with the disease. Several identified genes and chromosome locations play a role in the development of ulcerative colitis, Crohn's disease, or both. Genetic factors appear to be more important in Crohn's disease, although there is evidence that both conditions have some genetic defects in common.

In 2006, scientists identified variations in the interleukin-23 receptor (IL23R) as an important genetic link to both Crohnâ ' s disease and ulcerative colitis. Interleukin 23 is a cytokine that plays an important part in the inflammatory response and inflammatory diseases. Interestingly, scientists found that certain variations in the IL23 receptor gene can either increase or decrease the risk for inflammatory bowel disease.

Infections

Some studies have reported that children with IBD may have had more and earlier childhood infections. The measles virus has been of particular interest. However, according to the U.S. Centers for Disease Control and Prevention, and many studies, the measles virus does not cause Crohnâ ' s or IBD. In addition, studies conclusively report that the measles, mumps, and rubella (MMR) vaccine does not cause Crohnâ ' s disease, ulcerative colitis, or autism.

Dietary Factors

Inflammatory bowel disease is much more prevalent in industrialized nations and in higher-income groups. However, there is no strong evidence that diet or particular types of food cause Crohnâ ' s disease or ulcerative colitis.