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(American Journal of Pathology. 1998;153:1717-1722.)
© 1998 American Society for Investigative Pathology

Short Communications

Cryptosporidium parvum Initiates Inflammatory Bowel Disease in Germfree T Cell Receptor--Deficient Mice

Randy E. Sacco* , Joseph S. Haynes , James A. Harp , W. Ray Waters* and Michael J. Wannemuehler*

From the Veterinary Medical Research Institute* and Department of Veterinary Pathology, Iowa State University, and the USDA/Agricultural Research Service/National Animal Disease Center, Ames, Iowa

Flora-bearing mice with targeted disruption of T cell receptor (TCR)- or -ß genes spontaneously develop intestinal inflammation with features similar to ulcerative colitis in humans. TCR--deficient mice maintained germfree or colonized with a limited number of intestinal bacteria failed to develop inflammatory bowel disease (IBD)-like lesions. Evidently, inflammation in these mice does not develop spontaneously or result from a generalized antigenic stimulation, but rather requires induction by a heretofore unidentified specific stimulus. We describe the development of IBD-like lesions in germfree TCR--deficient mice monoassociated with the protozoan Cryptosporidium parvum. Lesions were seen in distal ileum, cecum, and colon and were most severe in the cecum. A prominent leukocytic infiltrate within the lamina propria was a common characteristic of the lesions observed in the C. parvum-infected germfree TCR--deficient mice. The leukocytic infiltrate was composed of aggregates of B220⁺ cells, the majority of which expressed surface IgD (ie, conventional B lymphocytes). It has been proposed that antigenic stimulation by a microorganism(s) is needed to initiate intestinal inflammation in TCR--deficient mice. Our results indicate that a single microbial species, C. parvum, is capable of triggering the development of IBD-like lesions in germfree TCR--deficient mice.

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