|Waters, W - IA STATE UNIV|
Submitted to: Research Workers in Animal Diseases Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: November 15, 1995
Publication Date: N/A
Technical Abstract: To further define the role of the T-cell in cryptosporidiosis, mice deficient in either the Alpha/Beta TCR or the gamma/delta TCR as well as C57BL-6 mice were orally inoculated with purified C. parvum. Mice were inoculated at 1 wk of age and examined at 8 wks of age (neonatal study) or inoculated at 8 wks of age and examined at 20 wks of age (adult study). TCR-Alpha deficient mice in the neonatal and adult studies had markedly thickened ceca due to elongated, hyperplastic glands. Gland lumina were filled with neutrophils, necrotic debris and cryptosporidia. Cecal lamina propria was expanded by infiltrates of lymphocytes, plasma cells, macrophages and neutrophils. Proximal colon was similarly but less severely affected. Typhlitis in the adult mice was more severe and extended to the muscular layer where lymphocytes and macrophages separated muscle fibers. Perivascular cuffs of inflammatory cells were seen in the mesentery with some sections containing granulomas. Vasculitis was present in some mesenteric vessels. Similar, but less severe lesions were seen in the proximal colon and distal ileum of adult mice. Lesions were not seen in delta-deficient mice or C57BL-6 controls. Thus, TCR-Alpha- deficient mice develop histopathologic lesions similar to those seen with human inflammatory bowel disease and may serve as a useful model for this disease.