Mice lacking the gene for inducible or endothelial nitric oxide are resistant to sporocyst induced Sarcocystis neurona infections.

The research article reveals that mice without the gene for inducible or endothelial nitric oxide are resistant to infections caused by the parasitic organism Sarcocystis neurona, which is known to commonly cause neurologic disorders in horses in the Americas.

Research Context and Objectives

• The research focuses on equine protozoal myeloencephalitis (EPM), a neurological syndrome commonly found in horses across the Americas, which is primarily caused by the apicomplexan parasite, Sarcocystis neurona.
• A significant area of this research is understanding the role of nitric oxide (NO), a biological mediator that is vital in the resistance against many intracellular parasites.
• The study aims to investigate the role of inducible and endothelial NO in resistance to the disease caused by S. neurona in mice.

Research Method

• The test subjects included interferon-gamma gene knockout (IFN-gamma-KO) mice, inducible nitric oxide synthase gene knockout (iNOS-KO) mice, endothelial nitric oxide synthase gene knockout (eNOS-KO) mice, and control mice (from the genetic backgrounds BALB/c or C57BL/6).
• These mice were divided into groups and subjected to oral feedings of sporocysts or Hanks balanced salt solution.
• The mice were monitored for signs of clinical disease and examined post-death.

Research Findings

• Clinical diseases and deaths were found to occur only among the IFN-gamma-KO mice.
• Microscopic lesions were found exclusively in the brains of IFN-gamma-KO mice.
• On the basis of these findings, the researchers concluded that inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) do not play a major role in resisting S. neurona infections.
• The study further suggests that IFN-gamma mediated immunity to S. neurona may be facilitated by mechanisms that do not depend on nitric oxide.