Page Banner

United States Department of Agriculture

Agricultural Research Service

Title: Accelerated Inflammatory Bowel Disease of Tcr-Alpha-Deficient Mice Persistently Infected with Cryptosporidium Parvum

Authors
item Waters, W - IA STATE UNIV., AMES, IA
item Palmer, Mitchell
item Ackermann, Mark
item Harp, James

Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 6, 1996
Publication Date: N/A

Interpretive Summary: Cryptosporidium parvum is an intestinal parasite that infects most mammals, including mice and cattle. Currently, there are no vaccines to prevent C. parvum infection of cattle. Studies using mice with genetic defects in their immune system enable us to better understand how an animal responds to an intestinal parasite such as C. parvum. In this study, we show that mice which have a genetic defect in their immune system develop thickened and inflamed intestinal tracts when infected with C. parvum. This information will give us a better understanding of the animal's response to C. parvum, and will aid in the development of a vaccine for cattle to protect them from this parasite.

Technical Abstract: TCR-alpha-deficient mice spontaneously develop inflammatory bowel disease (IBD) at 8 to 9 mos of age. This study characterizes an accelerated form of IBD induced by Cryptosporidium parvum infection. C. parvum-infected TCR-alpha-deficient mice developed IBD as early as 4 wk of age when challenged at 1 wk of age. The lesions of this accelerated IBD resembled the lesions of spontaneous IBD in TCR-alpha- deficient mice and consisted of a mononuclear cell infiltrate within the intestinal lamina propria and an increased proliferation of enterocytes. The monomuclear cells within the lamina propria consisted of B-cells and delta-gamma T-cells. The distal ileum, cecum, and colon were grossly thickened due to a pyperplastic mucosa and edematous submucosa. The mechanism by which C. parvum infection accelerates development of IBC is presently unclear.

Last Modified: 4/24/2014
Footer Content Back to Top of Page