Accelerated inflammatory bowel disease of TCR-alpha-deficient mice persistently infected with Cryptosporidium parvum

J Parasitol. 1997 Jun;83(3):460-4.

Abstract

TCR-alpha-deficient mice spontaneously develop inflammatory bowel disease (IBD) at 8-9 mo old. This study characterizes an accelerated form of IBD induced by Cryptosporidium parvum infection. Cryptosporidium parvum-infected TCR-alpha-deficient mice developed IBD as early as 4 wk old when challenged at 1 wk old. 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 mononuclear cells within the lamina propria consisted of B cells and gamma delta T cells. The distal ileum, cecum, and colon were grossly thickened due to a hyperplastic mucosa and edematous submucosa. The mechanism by which C. parvum infection accelerates development of IBD is presently unclear.

MeSH terms

  • Animals
  • Animals, Newborn
  • Cecum / pathology
  • Cell Division
  • Colon / pathology
  • Cryptosporidiosis / complications*
  • Cryptosporidiosis / immunology
  • Cryptosporidiosis / pathology
  • Cryptosporidium parvum*
  • Fluorescent Antibody Technique
  • Ileum / pathology
  • Inflammatory Bowel Diseases / etiology*
  • Inflammatory Bowel Diseases / immunology
  • Inflammatory Bowel Diseases / pathology
  • Intestines / immunology
  • Intestines / pathology*
  • Mice
  • Mice, Inbred C57BL
  • Receptors, Antigen, T-Cell, alpha-beta / deficiency*

Substances

  • Receptors, Antigen, T-Cell, alpha-beta