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Title:   Author  item
                                            WATERS, W - IOWA STATE UNIV., AMESitem
                                            Palmer, Mitchellitem
                                            WANNEMUEHLER, MICHAEL - IOWA STATE UNIV., AMESitem
                                            Sacco, Randyitem
                                            Harp, James
  Submitted to: Journal of Parasitology
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 2/18/2000
                                    Publication  Date: N/A
                                    Citation: N/AInterpretive Summary: Cryptosporidium parvum is a major cause of disease in newborn calves. Disease can also be transmitted to humans, especially through contaminated water.  In a large Cryptosporidium outbreak in Milwaukee, WI, several years ago, a number of people with inflammatory bowel disease (IBD) became infected with Cryptosporidium and experienced worsening of symptoms of  IBD.  In the present study, we used a mouse model to better understand the way in which Cryptosporidium infection might worsen IBD.  We found that B lymphocytes, the cells that produce protective antibodies against disease, are stimulated by the Cryptosporidium infection and contribute to the inflammation of the bowel seen in IBD.  These results help us to understand the role of Cryptosporidium in causing intestinal irritation and may aid in development of treatment for both humans and calves, thus benefiting both producers and consumers of beef and dairy products.
                                Technical Abstract: Mice with targeted disruptions in the T cell receptor alpha gene (TCRalpha-negative) spontaneously develop inflammatory intestinal lesions with extensive B cell lamina propria infiltrates.  Cryptosporidium parvum infection accelerates intestinal lesion formation in TCRalpha-negative mice.  In the present study, TCRalpha-negative mice were crossed with JH-ne ee (B cell deficient) mice and challenged with C. parvum to determine if B cells are required for intestinal lesion development. TCRalpha-negative x JH-negative mice challenged with C. parvum, either as neonates or adults, became persistently infected, whereas TCRalpha-positive -positive heterozygote control mice cleared the parasite. Cryptosporidium parvum colonized of TCRalpha-negative x JH-negative mice was heaviest in the distal ileum, with fewer parasites detected in the cecum and distal colon.  Despite persistent infection, TCRalpha-negative x  JH-negative mice did not develop inflammatory or hyperplastic intestinal lesions as detected in C. parvum-infected TCRalpha-negative mice.  These findings demonstrate that B cells are a necessary component for the development of inflammatory intestinal lesions of C. parvum-infected TCRalpha-negative mice.


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