Eosinophils Blamed for Food Allergies

Applied Genetics News,  April, 2001  

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A team of Cincinnati researchers has shown how eosinophils attack the digestive tract in a mouse model of food allergies. Their study appears in the April edition of Nature Immunology.

Eosinophils often appear in high numbers at sites of allergic inflammation, but it was not known if the cells caused the disease or were merely bystanders at the scene of the crime. "This study provides very clear evidence that, in this model, eosinophils play a critical role in disease," says Marshall Plaut, chief of the allergic mechanisms section at the National Institute of Allergy and Infectious Diseases (NIAID), which funded the study.

Marc Rothenberg, of Children's Hospital Medical Center in Cincinnati, directed a research team that developed a mouse model of gastrointestinal inflammatory diseases, which lead to weight loss, enlarged or inflamed digestive tissues, and the inability of food to move properly through the digestive tract.

To produce a food allergy in mice, lead author Simon Hogan first injected the animals with small amounts of ovalbumin, a harmless protein found in egg whites. The injections sensitized the mice to the protein, putting their immune systems on alert for future exposures. The researchers then fed the animals specially coated ovalbumin pellets that were designed to survive the acidic environment of the stomach. When the ovalbumin reached the small intestine it triggered an allergic reaction.

The animals became ill and lost weight as multiple regions of their digestive tracts became inflamed. Immune system proteins and cells rushed to the affected areas, and eosinophils accumulated in high numbers, particularly around damaged nerve cells. The walls of digestive organs swelled and food became stalled in the stomach.

In the sensitized mice, the presence of ovalbumin caused some of the cells lining the digestive tract to release eotaxin and attract eosinophils to the site. When the researchers repeated the experiment in mice that lacked the eotaxin gene, eosinophils did not appear and the mice did not develop the severe symptoms seen in normal mice.

By identifying eosinophils as a major cause of digestive inflammation, Rothenberg hopes to find new options for treating the disease. Several antieosinophil drugs are undergoing clinical trials for other diseases, and these might be effective agents to treat some food allergies. In addition, his mouse model of food- induced digestive illnesses should allow researchers to more thoroughly study related diseases and advance our knowledge of food sensitivities and allergies.

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COPYRIGHT 2001 Gale Group