Experimental models for ulcerative colitis.

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Animal model systems have been used extensively to study both experimental and naturally occurring ulcerative colitis syndromes. Interestingly, despite a variety of different animal species and a broad range of inducing agents, the response of the large intestine has been somewhat predictable. Although there is suggestive evidence for transmissible agents in several of these animal model systems, documentation of a bacterial or viral etiology has remained elusive. Perhaps the best evidence to suggest that bacteria play a role in the development of naturally occurring ulcerative colitis resides in the studies utilizing the rabbit-dinitrochlorobenzine model and the carrageenin-induced ulcerative colitis model in the guinea pig. The evidence for microbial involvement in these model systems includes the use of single bacterial species in the carrageenin model to produce an ulcerative colitis like disease and the use of antimicrobial agents to alter the experimental model system in the guinea pig and hamster with proliferative ileitis and evidence of transmissibility. Recent reports of transmissible agents for both ulcerative colitis and Crohn's disease in studies utilizing immunologically deficient mice also suggest that the search for the "agent" and mechanism should continue in model systems. The many differences between animal model systems and the human disease cannot be ignored. These differences make establishing what appears to be a complicated etiology even more difficult. Despite the difference in anatomy, physiology, and nutritional factors between animal model systems and the human disease process, the fact remains that one or more of these model systems may reflect the same mechanism or etiologic agent which occurs in the human disease.(ABSTRACT TRUNCATED AT 250 WORDS)