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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Ruminant Diseases and Immunology Research » Research » Publications at this Location » Publication #95427
Title: CRYPTOSPORIDIUM PARVUM-INDUCED INFLAMMATORY BOWEL DISEASE OF TCR-BETA X TCR-DELTA-DEFICIENT MICE

Author
item WATERS, W - IOWA STATE UNIV, AMES, IA
item WANNEMUEHLER, M - IOWA STATE UNIV, AMES, IA
item Sacco, Randy
item Palmer, Mitchell
item HAYNES, J - IOWA STATE UNIV, AMES, IA
item Pesch, Bruce
item Harp, James

Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/13/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary: Cryptosporidium is an intestinal parasite that causes diarrheal disease in many kinds of animals, including humans and newborn livestock, such as calves. In this study, we examined the effects of Cryptosporidium infection in mice that are deficient in certain types of lymphocytes; the immune cells that the body uses to fight infection. We found that Cryptosporidium infected these mice, and continued to grow in their intestines, eventually leading to bowel disease similar to that seen in some humans. Newborn calves are also deficient in some types of lymphocytes, which may explain why they are so susceptible to Cryptosporidium diarrhea. Understanding the effects of Cryptosporidium in animals lacking these lymphocytes will help in the design of vaccines and treatments for this costly disease.

Technical Abstract: Experimental challenge of neonatal immunocompetent strains of mice with Cryptosporidium parvum results in a transient, non-inflammatory enteric infection. However, challenge of mice deficient in alpha-beta and gamma-delta T cells (TCR-beta- x TCR-delta-deficient mice) with C. parvum resulted in persistent infection and severe inflammatory bowel disease (IBD). The most severe lesions in these mice were in the cecum with similar, yet less, severe lesions in the ileum and proximal colon. The most notable aspect of the histopathology was glandular hyperplasia with abscess formation, and extensive fibrosis of the lamina propria with infiltrates of predominantly polymorphonuclear cells and macrophages. Persistently-infected mice also developed extensive hepatic periportal fibrosis in association with C. parvum colonization of bile ducts. These findings indicate that neither gamma-delta T cells nor TCR-alpha-beta+ cells are necessary for the induction of IBD in alpha-beta T cell deficient mice experimentally challenged with C. parvum.