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Animal models of inflammatory bowel disease.

The human inflammatory bowel diseases, ulcerative colitis and Crohn's disease, remain enigmas in respect of their causes, whether or not they are separate entities or part of a spectrum, and the optimum means of treatment. As with other obscure diseases, investigators turn to animal models for a number of reasons, and three recent articles in the International Journal of Experimental Pathology have explored aspects of these models (Anthony A. et a/. 1995; Anthony D. et a/. 1995; Smith et a/. 1995). Similar naturally occurring diseases in animals may already have been explained aetiologically. Similar inflammatory states in animal gut, whether naturally occurring or experimentally induced, may be more readily investigated to identify key steps in the development and expression of gut disease than is possible in man. Finally, a very wide variety of therapeutic strategies can be piloted in animal models. The ideal model for exploitation for these aims should be effectively identical to one or other form of human inflammatory bowel disease, in respect of pathology, pathophysiology and symptomatology. It should occur in an animal species that is accessible, easy to maintain, immunologically similar to man, and manipulable in respect of exposure of the gut to infectious agents and other toxic factors. In the model it should be possible to alter gut commensal flora, dietary intake and aspects of immune status. In addition, the species should be acceptable, in terms of ethical aspects of animal experimentation, to the generality of the public. Clearly, we do not have such an animal model, but the assessment and exploitation of less perfect alternatives remains a growth industry. Consideration of any animal model involves the recognition that there are potentially two stages of any inflammatory response in the gut. After an initial episode of inflammation has been induced, there is a strong likelihood that the mucosal integrity of the gut will be, at least temporarily, altered (Hobson et a/. 1988,