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.