Colitis may be induced in animals by oral administration of sulfated polysaccharides (carrageenan, amylopectin sulfate, dextran sulfate), chemical irritation by rectal instillation of diluted acetic acid, delayed hypersensitivity reaction after sensitization to DNCB or after one single administration of TNBS, and Arthus reaction induced by intravenous injection of immune complexes after chemical irritation of the colon, and by chemoattractant peptides such as FMLP. It appears that all models of colon inflammation in the rat, mouse, or rabbit produce increased amounts of eicosanoids similar to that found in human colitis. Thus, animal studies provide useful information on the origin, regulation, and function of inflammatory mediators. However, with the possible exception of the cotton-top tamarin, no animal model of induced or spontaneous inflammation of the colon is analogous to human ulcerative colitis in etiology, course of disease activity, or histology (114). The observation that two different immune-mediated models gave similar results suggests that the colitis is not a specific response to delayed-type hypersensitivity or immune-complex-mediated reactions but rather an unspecific, stereotype response (125). The original disturbance may not determine the nature of the lesions ultimately produced but may instead serve as an initiator of a final common immunologic pathway.

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