Inflammatory bowel disease (IBD) is characterized by persistent chronic inflammation of the bowel wall. Although the disease is currently treated with anti-inflammatory medications, the underlying mechanisms of the disease are poorly understood. Lipoxins are novel lipid mediators derived from arachidonic acid that possess powerful anti-inflammatory effects on neutrophil function. These messengers are produced late in an inflammatory response and their presence serves to resolve inflammation. Since these mediators are produced in intestinal mucosa, we hypothesized that IBD may be caused, in part, by a failure to resolve inflammation by a defect in lipoxin synthesis or metabolism. Seemingly innocuous inflammatory stimuli, such as gut bacteria or food antigens, may result in runaway inflammation without anti-inflammatory mediators to resolve the initiated response.