Author
Waters, Wade | |
HAYNES, J - IOWA STATE UNIV., AMES | |
WANNEMUEHLER, M - IOWA STATE UNIV., AMES | |
Harp, James | |
Sacco, Randy |
Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only Publication Acceptance Date: 4/19/1998 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: Cryptosporidium parvum is an intracellular protozoan parasite that causes diarrheal disease in various mammals, including humans. The disease is most severe in immunocompromised individuals. TCR-alpha-deficient mice spontaneously develop inflammatory bowel disease (IBD) at 3-4 months of age. The onset of IBD in these mice is greatly accelerated by infection with C. parvum. Germ-free TCR-alpha-deficient mice do not develop IBD. In this study, we infected germ-free and flora bearing TCR-alpha-deficient mice with C. parvum. Germ-free TCR-alpha-deficient mice were more heavily infected than flora-bearing mice, as evidenced by greater numbers of oocysts shed in feces and greater numbers of parasites detected on histologic sections. In addition, germ-free TCR-alpha-deficient mice developed IBD with lesions similar to those detected in flora bearing TCR-alpha-deficient mice infected with C. parvum. IBD lesions in germ- free TCR-alpha-deficient mice had sharply delineated foci of lymphocytic infiltrates (predominantly B220+ and IgD+) within the lamina propria. Distal ileum, cecum, and colon were involved, but inflammation was most severe in the cecum of both germ-free and flora-bearing mice. These results indicate that infection with C. parvum is sufficient to initiate IBD in germ-free TCR-alpha-deficient mice. (Supported by NIH DK52552) |