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Infection and Immunity, April 2007, p. 1745-1750, Vol. 75, No. 4
0019-9567/07/$08.00+0 doi:10.1128/IAI.01528-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Division of Infectious Disease, Wadsworth Center, New York State Department of Health, Albany, New York 12208
Received 22 September 2006/ Returned for modification 26 October 2006/ Accepted 4 January 2007
The development of small-animal models is necessary to understand host responses and immunity to emerging infectious diseases and potential bioterrorism agents. In this report we have characterized a murine model of intestinal ricin intoxication. Ricin administered intragastrically (i.g.) to BALB/c mice at doses ranging from 1 to 10 mg/kg of body weight induced dose-dependent morphological changes in the proximal small intestine (i.e., duodenum), including widespread villus atrophy and epithelial damage. Coincident with epithelial damage was a localized increase in monocyte chemotactic protein 1, a chemokine known to be associated with inflammation of the intestinal mucosa. Immunity to intestinal ricin intoxication was achieved by immunizing mice i.g. with ricin toxoid and correlated with elevated levels of antitoxin mucosal immunoglobulin A (IgA) and serum IgG antibodies. We expect that this model will serve as a valuable tool in identifying the inflammatory pathways and protective immune responses that are elicited in the intestinal mucosa following ricin exposure and will prove useful in the evaluation of antitoxin vaccines and therapeutics.
Published ahead of print on 5 February 2007.
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