The exact cause of IBD is not fully understood. Processes thought to be involved in its development include genetic predisposition, dysregulation of the inflammatory response within the GI tract, or perhaps environmental or antigenic factors.3,4 The fact that a positive family history is a strong predictor of IBD supports the theory that genetic predisposition may be responsible in many cases. Many potential candidate genes have been identified. An example is a gene found on chromosome 16 that encodes for nucleotide oligomerization domain 2 (NOD2). NOD2 is a cytoplasmic protein expressed in macrophages, monocytes, and gut epithelial cells thought to be involved in recognition and degradation of bacterial products by the gut wall. Less is known about genetic alterations that may predispose patients to UC, but UC may share common genetic features with CD.

An alteration in the inflammatory response regulated by intestinal epithelial cells may also contribute to development of IBD. This may involve inappropriate processing of antigens presented to the GI epithelial cells.3,4,10,11 The inflammatory re sponse in IBD may actually be directed at bacteria that normally colonize the GI tract. Products derived from these bacteria may translocate across the mucosal layer of the GI tract and interact with various cells involved in immunologic recognition. The result is T-cell stimulation, excess production ofproinflammatory cytokines, and persistent inflammation within the GI tract.

The intestinal mucosa of patients with CD has a preponderance of CD4+ type 1 helper T cells, while patients with UC have more CD4+ lymphocytes with atypical type 2 helper T cells.1 Likewise, drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs) that disrupt the integrity of the GI mucosa may facilitate mucosal entry of intestinal antigens and lead to disease flares in patients with IBD.12

The role of antigens derived from dietary intake in the development of IBD is less well defined. There is some speculation that ingestion of large quantities of refined carbohydrates or margarine leads to higher rates of CD. Use of oral contraceptives has been associated with increased development of IBD in some cohort studies, but a strong causal relationship has not been proven.8

Lastly, positive smoking status has been shown to have protective effects in UC, leading to reductions in disease severity. The opposite is true in CD, as smoking may lead to increases in symptoms or worsening of the disease.10

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