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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 #62401

Title: CRYPTOSPORIDIUM PARVUM INFECTION IN TCR-ALPHA- AND TCR-DELTA-DEFICIENT MICE

Author
item WATERS, W - IA STATE UNIV., AMES, IA
item Harp, James

Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/1/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary: Cryptosporidium parvum is a single-celled parasite which infects various mammals, including humans, cattle and mice. This parasite is a significant cause of diarrhea in calves and humans. The disease in humans is often associated with outbreaks due to contaminated water supplies. These water supplies are often contaminated by runoff from pastures inhabited by infected calves. Thus, control of the infection in calves could lead to decreased infections in man. To develop control measures in calves, we must first determine how the parasite is controlled by its host. These types of studies often utilize mice as a model for the disease in calves or humans. From prior studies, it is clear that immune cells are necessary to fight off infection with C. parvum. The types of immune cells and modes of action of these immune cells are not clear. This study identified two types of immune cells involved in the control of the parasite by mice. The way in which these two types of immune cells work were shown to be distinctly different. Also, a possible model for an important human disease (inflammatory bowel disease) was discovered.

Technical Abstract: Neonatal mice deficient in either alpha/beta or gamma/delta T-cells were more susceptible to infection with the protozoan parasite, Cryptosporidium parvum, than were control mice. Furthermore, alpha/beta T-cell-deficient neonatal mice were unable to clear the parasite and developed a chronic infection. Gamma/delta T-cell- deficient neonatal mice had an increased duration of infection as compared to control mice, but were able to clear the infection. Adult alpha/beta T-cell-deficient mice were also susceptible to C. parvum, whereas adult control and gamma/delta T-cell-deficient mice were not. As with the neonates, adult alpha/beta T-cell-deficient mice were unable to clear C. parvum once infected. In addition, C. parvum infection of alpha/beta T-cell-deficient mice resulted in accelerated development of an inflammatory bowel disease-like syndrome often seen in aging mice of this strain.