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Inflammatory Bowel Disease (Crohn’s and Ulcerative Colitis)

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Anatomy of the Digestive Tract and Immunology of Inflammatory Bowel Disease

The digestive tract consists of a single long tube that has many folds and convolutions and extends from the mouth to the anus. The tube is divided into distinct parts (such as the esophagus, stomach, small intestine, and large intestine), each with a specific structure and function. Solid organs such as the liver and pancreas are also considered portions of the digestive system.

The hollow parts are responsible for breaking down large portions of food into small molecules that can be readily absorbed into the circulation. The sterile bloodstream is separated from the mass of nutrients, toxins, and organisms in various parts of the hollow digestive tract by only a very thin layer of cells, collectively called the intestinal mucosa. This delicate and complex lining is responsible for secreting substances that aid in digestion and absorption of nutrients, and for defending the body against the toxins and other contaminants in the intestine itself.

The intestinal mucosa must selectively allow entry of beneficial molecules while excluding toxins and organisms that could be harmful. To do this, the mucosa is equipped with several kinds of cells including secretory cells that produce a layer of mucus to trap contaminants, immune cells that directly attack and destroy invading organisms (macrophages), and other inflammatory cells (neutrophils, killer T cells, and others) that respond to the presence of foreign molecules by producing proinflammatory cytokines (small cell-signaling protein molecules) (Abraham 2009).

During healthy conditions, the immune cells in the intestinal lining cope with invaders quickly and efficiently, without producing excessive amounts of localized inflammation. However, in inflammatory bowel disease, inflammation becomes uncontrolled. Cytokines released by inflammatory cells in the intestine attract additional immune cells that produce destructive chemicals and propagate inflammation (Neuman 2004). In particular, a subset of inflammatory immune cells called Th17 cells are principally responsible for driving inflammation in Crohn’s disease, while Th2 cells drive inflammation in ulcerative colitis. A number of factors cause Th17 and Th2 cells to produce excessive inflammation including penetration of the intestinal epithelium by gut microbes, composition of the intestinal microbiota, injury to the intestinal wall, insufficient mucus layer production, and allergies or sensitivities to foods. Genetics contribute to inflammatory bowel disease susceptibility, but the immune response as well as the intestinal microenvironment and diet can be modified to mitigate inflammatory propensity, even in genetically predisposed individuals.

Since the inflammatory reactions taking place in the gut can promote systemic inflammation people with IBD should monitor levels of inflammatory cytokines in their blood. Cytokine testing can be used as a measure of the effectiveness of anti-inflammatory therapies, and can also help determine risk for other conditions associated with inflammation, such as atherosclerosis. Cytokine blood profiles measure tumor necrosis factor-alpha (TNF-α), interleukin-1 (beta) (IL-1b), and interleukin-6 (IL-6).