Ulcerative colitis
Description
An in-depth report on the causes, diagnosis, treatment, and prevention of ulcerative colitis.
Alternative Names
Inflammatory bowel disease; Colitis - ulcerative
Causes
Inflammatory bowel disease is due to many causes. Often, genetic problems in the intestine enable viruses or bacteria to trigger an immune response that causes inflammation and injury in the intestines. In IBD, the defense systems appear to be impaired, because of either defects in the mucosal lining that provides a barrier in the intestine or an inability to make repairs after injury.
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 cell
s 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.
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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.
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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 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 appears to occur in IBD, although each disorder has a different balance:
-
Patients with ulcerative colitis favor a TH2 response, which activates the interleukins IL-5, IL-6, and IL-10. These proteins affect mostly 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. These substances 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. Interleukin 6 inhibits a natural mechanism called apoptosis, a process in which 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). ICAM-1 plays a role in 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 - 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.
Infections
One theory suggests that viruses or bacteria within the intestine may alter properties in the lining and intestinal tract. Over time, these changes may trigger the injurious processes that lead to inflammatory bowel disease. Some studies report 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 many studies, the measles virus does not cause Crohn’s or IBD. In addition, studies conclusively report that the measles, mumps, and rubella (MMR) vaccine does not cause Crohn’s disease, ulcerative colitis, or autism.
Dietary Factors
Inflammatory bowel disease is much more prevalent in industrialized nations and in higher-income groups. Experts believe that diet must play some role, although studies have been conflicting over its importance.
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Review Date: 8/23/2006
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Reviewed By: Harvey Simon, M.D., Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital
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