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Crohn's Disease: Inflammatory Bowel Disease


An in-depth report on the causes, diagnosis, treatment, and prevention of Crohn's Disease.

Alternative Names

Cramps (Menstrual); Inflammatory Bowel Disease; Irritable Bowel Syndrome


The cause of inflammatory bowel disease is multifactoral. It is due in many cases to a genetic susceptibility that enables an agent such as a virus or bacteria to trigger an abnormal immune reaction, which in turn, causes an inflammatory response in the intestines. Although Crohn's disease (CD) has features that resemble an autoimmune disease (in which the body's immune system attacks its own cells), some researchers posit that CD may be due to initial immune deficiencies.

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, which are separate agents 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 (TH 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 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 are directed against the body's own cells.
  • TH-cells also secrete or stimulate the production of powerful immune factors called cytokines. In small amounts, cytokines are indispensable for healing. If overproduced, however, they can cause serious damage, including inflammation and cellular injury. 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 appear to occur in IBD, although each disorder has a different balance:

  • Ulcerative colitis patients favor a Th2 response, which activates the interleukins IL-5, IL-6, and IL-10, which mostly affect mucosal areas in the intestine.
  • Research indicates that Crohn's disease patients have increased activity in Th1 helper cells, which activates interleukin-2 (IL-2) and interferon-gamma, which affect intestinal cells. Tumor necrosis factor may be a particularly potent immune factor in Crohn's disease. It is important in properties that regulate inflammation and cell proliferation. If genetic or other factors increase production of this immune compound, it can lead to great harm.

Interleukin 6 appears to play a part in both IBDs, by inhibiting a natural mechanism called apoptosis, a process whereby cells self-destruct. In such cases, cells proliferate faster than they die, causing an excessively strong immune response.

Adhesion Molecules. Increased levels of certain molecules called E-selectin and intercellular adhesion molecule-1 (ICAM-1) also appear to play a major role in the inflammatory process by causing damaging immune factors to accumulate on intestinal cells. E-selectin may be involved in the early stages of the disease (especially ulcerative colitis) and ICAM-1 in the persistence of either inflammatory bowel disease.

Matrix Metalloproteinase. Greater activity of enzymes called matrix metalloproteinase has been detected in the colons of patients with IBD. Such increased levels tend to break down the extracellular matrix, a barrier composed of structural proteins and elastic fibers that surrounds and supports cells, in this case in the colon. Researchers suggest that this activity may cause persistent damage once the inflammatory process has triggered IBD.

Genetic Factors

Although the causes of inflammatory bowel disease are not yet known, genetic factors certainly play some role. Between 10% and 20% of people with ulcerative colitis have family members with the disease. A number of candidate genes and chromosome locations have been identified that might prove to 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 they may have genetic defects in common. In either case, multiple genetic factors are likely to be responsible for susceptibility to these disorders.

Specific Genes Involved. One of the most important genetic discoveries to date was the identification of a genetic variant called NOD2, which appears to alter the immune system so that it launches an over-reaction in response to bacteria, causing inflammation. This genetic factor might be involved in 15% of Crohn's disease cases. Those with one copy of the mutated gene had twice the average risk of developing Crohn's, and those with two defective genes faced 20 to 40 times the risk.

Infectious Agents

Evidence now suggests that viruses or mycobacteria within the intestine may alter properties in the lining and intestinal tract, which over time triggers the injurious processes leading to inflammatory bowel disease. For example, some studies have found that children with IBD are likely to have had more and earlier childhood infections, so a number of specific childhood infectious agents have become a focus of some interest.

Measles. Some studies have found that children with IBD are likely to have had more and earlier childhood infections, so a number of specific childhood infectious agents have become a focus of some interest. The measles virus is of particular interest. One small study reported an association between wild strains of the virus and Crohn's disease patients.

Much publicity has centered on a possible link between the vaccine for measles (the MMR) and a variant of autism that includes inflammatory bowel disease (IBD) and impaired behavioral development. Such findings have been rigorously reviewed and refuted in a number of well-conducted studies. Of special note, a 2002 analysis of vaccination records found no higher incidence in autism, with or without behavioral problems and gastrointestinal disorders. In the study, there was a link between impaired behavioral development and bowel problems, but they were not related to the vaccine. The popular media has incorrectly reported the possible link between autism and MMR as causing a split in the scientific community, but virtually all experts refute any association. In fact, reports of symptoms related to autism increased only after widespread publicity of this supposed side effect.

Mycobacteria. Another suspect for Crohn's disease may be mycobacteria that cause a form of tuberculosis.

Escherichia coli. The intestine normally harbors E. coli bacteria. In most cases the bacteria are harmless and even protective. Some E. coli strains however can be damaging, and some have been identified in Crohn's disease that bind excessively to the intestinal walls and can penetrate the lining.

Cytomegalovirus. Cytomegalovirus (CMV) is a common virus that is also under suspicion as a contributor to severe cases of IBD.

Dietary Factors

Inflammatory bowel disease is much more prevalent in industrialized nations and in higher-income groups. Experts believe, then, that diet must play some role, although studies have been conflicting over its importance.


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