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Title:   Author  item
                                            SONEA, IOANA - IOWA STATE UNIV., AMESitem
                                            Palmer, Mitchellitem
                                            Harp, James
  Submitted to: Clinical and Diagnostic Laboratory Immunology
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 10/26/2001
                                    Publication  Date: N/A
                                    Citation: N/AInterpretive Summary: Cryptosporidium parvum is an intestinal parasite that causes diarrheal disease in calves.  This disease is costly to dairy and beef producers, and the disease can also spread to humans by contaminated water and food. In previous studies, we showed that C. parvum infection could trigger the development of inflammatory bowel disease (IBD), which can affect both  humans and animals.  In this study, we found that inflammation resulting from C. parvum infection could be reduced by blocking the action of molecules that carry signals from the nervous system.  These findings help to clarify the interactions of the nervous and immune systems in regulating disease.  This information underscores the importance of controlling stress in domestic animals in order to reduce disease and increase profitability for producers.
                                Technical Abstract: Inflammatory bowel disease (IBD) is a chronic, debilitating disorder of uncertain and perhaps multiple etiologies.  It is believed to be due in part to disregulation of the immune system.  Neuroimmune interactions may be involved in induction or maintenance of IBD.  In the present study, we examined the potential role of a neurotransmitter, Substance P in a mouse  model of IBD.  We found that receptors for Substance P were upregulated in intestinal tissue of mice with IBD-like syndrome.  Dosing of mice with LY303870, a Substance P antagonist, reduced the severity of IBD, and treatment of mice with pre-existing IBD allowed partial healing of lesions.  We hypothesize that blocking the binding of Substance P to its intestinal receptor interrupts the inflammatory cascade that triggers and maintains intestinal lesions of IBD.


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