In general, mouse models of colitis are used to study its pathophysiology and for the development of new treatment modalities for inflammatory bowel disease (IBD). For the latter it is essential to select a mouse model that has many overlapping features with human IBD.
More than 50 experimental colitis models have been developed and they have provided us with very useful insights into IBD physiology, as reviewed by Bouma and Strober1 and others,2–4 but they have limited use in predicting the clinical relevance of therapeutic targets in IBD.5
Experimental colitis models broadly fit into four different groups. First is spontaneous colitis, resulting from a naturally occurring genetic abnormality. Second is induced colitis occurring as a consequence of a targeted mutation or the introduction of a transgene. Third is induced colitis resulting from administration of different exogenous causative agents. Fourth is induction of colitis by manipulation of the immune system. We have learned a great deal from these models about the involvement of genetics, the microbiota and the role of different cells and the mucus layer in the development of IBD.
Here we discuss the major mistakes that are made using experimental colitis models, based on our own experience and the scientific literature. Recently increased awareness has developed for the necessity to improve the methodological quality of animal studies.