Author
Palmer, Mitchell | |
WATERS, R - IA STATE UNIVERSITY | |
Ackermann, Mark | |
Harp, James |
Submitted to: American College of Veterinary Pathologists Abstracts
Publication Type: Abstract Only Publication Acceptance Date: 12/6/1996 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: TCR(alpha)deficient mice develop a spontaneous inflammatory bowel disease-like syndrome beginning at 3-4 months of age. To examine the effect of C. parvum infection on the development of the IBD-like syndrome, TCR(alpha)deficient mice, TCR(delta)deficient mice, and C57BL-6 mice were orally inoculated with C. parvum. TCR(alpha)deficient mice became persistently infected and developed inflammatory lesions as early as 4 wks of age. Lesions included: 1) markedly thickened ceca due to elongated hyperplastic glands, 2) increased enterocyte proliferation as measured by expression of proliferating cell nuclear antigen, 3) crypt abscesses, 4) expanded cecal lamina propria due to infiltrates of B-cells and gamma delta T-cells. Lesion severity increased with duration of infection, eventually extending to all layers of the cecal wall and accompanied by fasculitis and granulom formation. Lesions were not seen in TCR(delta)deficient, C57BL-6, or non-infected TCR(alpha)deficient mice. Thus, TCR(alpha)deficient mice develop an IBD-like syndrome at an accelerated rate following infection with C. parvum. |