Foals are Interferon-Gamma Deficient at Birth

Newborn foals are deficient in a certain protein released by white blood cells that is essential for protection against the bacterium Rhodococcus equi and other pathogens, stated scientists at the University of Kentucky's Gluck Equine Research Center. Pneumonia caused by R. equi can be costly to treat, and fatal.

The researchers collected blood samples from a group of foals at regular intervals during their first six months of life, and blood and bronchoalveolar lavage samples from another group of foals at one, three, or six months of age. They looked for expression of interferon-gamma (IFNg), which is produced by certain white blood cells (called T-lymphocytes) and which fights viral infection by preventing virus multiplication.

"Why are young foals susceptible to different diseases, particularly R. equi?" questioned David Horohov, PhD, William Robert Mills Chair and professor at Gluck. "We do know based on the work of Dr. Steve Hines (of Washington State University) and Dr. Steeve Giguere (of the University of Florida) that adult horses are resistant to Rhodococcus in part because they produce a lot of INFg, the cytokine that determines resistance. Foals, however, are basically incapable of expressing the gene for IFNg."

Horohov said a preliminary study completed on farms with endemic R. equi in Illinois agrees with the Gluck research: The foals with the lowest levels of IFNg at birth were more likely to become infected with R. equi.

While Horohov isn't sure why some foals show this inability to fight R. equi and other pathogens, he knows that foals begin approaching normal adult levels of IFNg production by approximately three months of age. Why foals' immune systems are incapable of producing molecules necessary for stimulating a cell-mediated response might be traced back to the maternal environment during pregnancy. A similar reduction in maternal immune function is seen during pregnancy, probably in order to maintain the pregnancy and not reject the developing fetus.

Regardless of where these deficits arise, Horohov says it makes sense to try to boost a cell-mediated response (in the cells) to disease challenge rather than simply boost a humoral (in the blood) response (by increasing circulating antibody levels). Boosting humoral response has been the aim of R. equi treatments until now.

Horohov and his colleagues are examining whether common immunomodulators can accelerate the young foal's ability to produce IFNg, which could protect the foals from the disease. "Though we can draw inferences from what we see on endemic farms, we're going to need to develop a challenge model to test our hypothesis that IFNg plays a central role in resistance to R. equi in young foals," said Horohov.

About the Author

Stephanie L. Church, Editor-in-Chief

Stephanie L. Church, Editor-in-Chief, received a B.A. in Journalism and Equestrian Studies from Averett College in Danville, Virginia. A Pony Club and 4-H graduate, her background is in eventing, and she is schooling her recently retired Thoroughbred racehorse, Happy, toward a career in that discipline. She also enjoys traveling, photography, cycling, and cooking in her free time.

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