Accelerated inflammatory bowel disease of TCR-alpha-deficient mice persistently infected with Cryptosporidium parvum.
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.
Waters
W R
WR
U.S. Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Ames, Iowa 50010-0070, USA.
Palmer
M V
MV
Ackermann
M R
MR
Harp
J A
JA
D000818:Animals; D000831:Animals, Newborn; D002432:Cecum / Q000473:pathology; D002455:Cell Division; D003106:Colon / Q000473:pathology; D003457:Cryptosporidiosis / Q000150:complications* / Q000276:immunology / Q000473:pathology; D016785:Cryptosporidium parvum; D005455:Fluorescent Antibody Technique; D007082:Ileum / Q000473:pathology; D015212:Inflammatory Bowel Diseases / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D007422:Intestines / Q000276:immunology / Q000473:pathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000172:deficiency*
D016693:Receptors, Antigen, T-Cell, alpha-beta