Skip to main content
ARS Home » Research » Publications at this Location » Publication #125895
Title: MICE LACKING THE GENE FOR INDUCIBLE OR ENDOTHELIAL NITRIC OXIDE ARE RESISTANT TO SPOROCYST INDUCED SARCOCYSTIS NEURONA INFECTIONS

Author
item ROSYPAL, ALEXA - VIRGINIA TECH
item LINDSAY, DAVID - VIRGINIA TECH
item DUNCAN, JR., ROBERT - VIRGINIA TECH
item AHMED, S. - VIRGINIA TECH
item ZAJAC, ANNE - VIRGINIA TECH
item Dubey, Jitender

Submitted to: Veterinary Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/9/2001
Publication Date: N/A
Citation: N/A

Interpretive Summary: Sarcocystis neurona is a single-celled parasite that causes a fatal disease in horses (EPM). Little is known of the pathogenesis of EPM because there is no suitable animal model for it. Certain cytokines (substances released by lymphocytes) are considered important mediators of immunity to parasites. Scientists at the Beltsville Agricultural Research Center and the Virginia Tech, Blacksburg, Virginia have found that nitric oxide release is not a mechanism involved in the pathogenesis of EPM. These results will be of interest to biologists, parasitologists and immunologists.

Technical Abstract: Equine protozoal myeloencephalitis (EPM) is a neurologic syndrome in horses from the Americas and is usually caused by infection with the apicomplexan parasite, Sarcocystis neurona. Little is known about the role of immunobiological mediators to this parasite. Nitric oxide is important in resistance to many intracellular parasites. We therefore investigated the role of inducible and endothelial nitric oxide in resistance to clinical disease cause by S. neurona in mice. Groups of interferon-y gene knockout (IFN-y-KO) mice, inducible nitric oxide synthase gene knockout (eNOS-KO) and appropriate genetic background mice (BALB/c or C57BL/6) were orally fed sporocysts of Hanks balanced salt solution. Mice were observed for signs of clinical disease and at necropsy. Clinical disease and deaths occurred only in the IFN-y-KO mice. Results of this study indicate that iNOS and eNOS are not major mediators of resistance to S. neurona infections. Results of this study suggest that IFN-y mediated immunity to S. neurona may be mediated by non-nitric oxide dependent mechanisms.