Interferon gamma protective against Sarcocystis neurona encephalitis in susceptible murine model.

The study explores the protective effect of the cytokine, interferon gamma (IFNγ), against Sarcocystis neurona encephalitis, a disease affecting horses, as observed in mouse models. It reveals that IFNγ is crucial in warding off the disease, highlighting the significant role of T-lymphocytes in controlling S. neurona encephalitis.

Exploring Sarcocystis neurona encephalitis

• Sarcocystis neurona is the primary cause of an infectious equine disease known as equine protozoal myeloencephalitis (EPM) which affects the neurological functions of horses.
• The research has focused on understanding the immune response of horses to the infection, as well as the discrepancy in the frequency of exposure to the protozoa and instances of the actual disease.
• Horse models are challenging to study in disease investigations, and therefore mouse models are used.

Role of Interferon Gamma (IFNγ)

• IFNγ appears to play a key protective role against S. neurona encephalitis. Mice lacking this cytokine are found to be highly susceptible to the disease.
• This research however aims to clear the existing confusion regarding the susceptibility of lymphocyte-deficient mice, which lack T-lymphocytes and correspondingly the production of IFNγ, to this disease.

Investigation in Different Mice Strains

• The researchers studied S. neurona disease susceptibility in two different lymphocyte-deficient mouse strains, C57Bl/6 (B6) scid and Balb/c scid. B6 mice were found to be susceptible to S. neurona encephalitis, as 100 percent of infected mice developed the disease within 60 days of infection.
• In contrast, Balb/c.scid mice showed a high resistance to the disease with only 10 percent developing neurological symptoms within the same timeframe.
• Post-infection examinations of the cerebellar tissues confirmed the presence of S. neurona in B6.scid mice but not in Balb/c.scid mice.

Impact of T-lymphocyte-derived IFNγ

• IFNγ-competent T-lymphocytes were introduced into B6.scid mice, and this adoption provided full protection against S. neurona encephalitis.
• However, when IFNγ-deficient T-lymphocytes were introduced, the recipient mice continued to be susceptible to the disease.

The results of these studies confirm that the mouse strain is crucial when investigating susceptibility to S. neurona disease. The evidence overwhelmingly suggests that T-lymphocytes producing IFNγ play a protective role in mice susceptible to S. neurona encephalitis.