ases are in terms of symptoms, their underlying physiology is vastly different. Drugs on the market for treating acid reflux do not abate the symptoms of EE, which is not caused by production of stomach acid, but likely by inflammation in the esophagus resulting from the abnormal accumulation of immune cells know as eosinophils--hence its name eosinophilic esophagitis. Eosinophils are white blood cells that contain inflammatory chemicals, highly reactive proteins, destructive enzymes, toxins, muscle contractors and signaling molecules that can guide immune defenses to the site of infection.

At the Cincinnati Children's Hospital Medical Center, Professor of Pediatrics Marc E. Rothenberg, M.D., Ph.D., has seen patients with EE for a number of years and pursued clinical and laboratory research on the disease as well. To better understand the disease, Dr. Rothenberg and his colleagues examined the gene expression in tissue samples taken directly from the esophagus of individuals with EE as well as from people without the disease. These individuals were selected to represent a diverse sample with respect to age, sex and disease state. Dr. Rothenberg and his colleagues found that a particular set of 574 genes were expressed differently in people with EE from people without the illness.

This transcript signature, as they call it, yielded some surprising findings; it was largely the same for every person with EE, regardless of age and whether or not these people had food allergies. This transcript signature was quite distinct from the signature observed in patients with acid reflux disease, thus allowing the two diseases to be easily discriminated. Although EE is more common in males than in females, the genes expressed in the esophagus did not vary dramatically between males and females with EE. Of the 574 genes, the investigators found that the expression of one gene in particular, termed eotaxin-3, was elevated in people with EE compared to people without
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Contact: Jason Socrates Bardi
jbardi@niaid.nih.gov
301-402-1663
NIH/National Institute of Allergy and Infectious Diseases
1-Feb-2006

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