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

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1998-12-01
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Sacco, Randy
Harp, James
Waters, W. Ray
Wannemeuhler, Michael
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Haynes, Joseph
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Veterinary Pathology
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Flora-bearing mice with targeted disruption of T cell receptor (TCR)-α or -β genes spontaneously develop intestinal inflammation with features similar to ulcerative colitis in humans. TCR-α-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-α-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-α-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-α-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-α-deficient mice.

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This article is published as Sacco, Randy E., Joseph S. Haynes, James A. Harp, W. Ray Waters, and Michael J. Wannemuehler. "Cryptosporidium parvum initiates inflammatory bowel disease in germfree T cell receptor-α-deficient mice." The American journal of pathology 153, no. 6 (1998): 1717-1722. doi: 10.1016/S0002-9440(10)65686-6. Posted with permission.

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