Campus Units

Veterinary Pathology

Document Type

Article

Publication Version

Published Version

Publication Date

12-1998

Journal or Book Title

The American Journal of Pathology

Volume

153

Issue

6

First Page

1717

Last Page

1722

DOI

10.1016/S0002-9440(10)65686-6

Abstract

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.

Comments

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.

Rights

Works produced by employees of the U.S. Government as part of their official duties are not copyrighted within the U.S. The content of this document is not copyrighted.

Language

en

File Format

application/pdf

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