Experimental models of inflammatory bowel disease

Etiology of inflammatory bowel disease (IBD) is still unknown. A lot of experimental models of these diseases have been developed during the last years. They can be classified as spontaneous and induced models. Spontaneous models are infectious, genetic or of unknown etiology. Induced models are infectious, immune-mediated, chemical or genetic. All these models share some characteristics with IBD. In general, they are characterized by a chronic inflammation of the gut, and often, this inflammation appears secondary to mucosal abnormalities leading to an abnormal immune and inflammatory response toward luminal material. The most interesting models are thus those that share not only clinical and pathological characteristics with IBD, but also early mucosal abnormalities. From that point of view, the nonsteroidal anti-inflammatory drug (NSAID) enteropathy is probably one of the most interesting model for Crohn's disease (CD). In effect, this model shares an early modification with CD, that is increased intestinal permeability. In animals NSAID enteropathy, the increased intestinal permeability appears early after NSAID administration and is followed by inflammatory lesions. These lesions seem to be secondary to the increased permeability and depend on intraluminal materials, such as alimentary antigens or bacterial fragments. A possible link between the increased permeability and the inflammatory lesions could be an abnormal immune and inflammatory response toward the intraluminal materials. If the increased intestinal permeability in CD was confirmed, the same mechanisms could be implicated in its pathophysiology.