Nutrition

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Sensitivities to foods, as experienced with irritable bowel syndrome (IBS), may start with immune responses caused by earlier bouts of gastrointestinal infection.

Scientists at KU Leuven, Belgium, found that when a gastrointestinal infection was present in the guts of mice at the same time as a specific food protein, the mice developed a sensitivity to the food protein.

The team infected mice with the stomach bug Citrobacter rodentium, which mimics E. coli infection in humans, and at the same time fed them ovalbumin, a protein found in egg white.

When the mice were given ovalbumin after the infection cleared, they were found to tolerate it less and experience abdominal pain. Histamine was also released — a sign that the immune system had been activated. However, the immune response only occurred in the part of the intestine that had been infected by the disruptive bacteria and did not produce more general symptoms of a food allergy.

Mice given ovalbumin but not infected with the bug did not experience these symptoms.

Because IBS can develop after a gastrointestinal infection such as food poisoning, the team had set out to discover what makes a once-healthy gut become compromised. In a healthy intestine, they said, the immune system does not react to foods.

According to the authors, up to 20% of the world’s population suffers from IBS but the condition is not fully understood.

“Very often these patients are not taken seriously by physicians, and the lack of an allergic response is used as an argument that this is all in the mind, and that they don’t have a problem with their gut physiology,” says lead author Professor Guy Boeckxstaens, a gastroenterologist at KU Leuven. “With these new insights, we provide further evidence that we are dealing with a real disease.”

The researchers then went on to see if people with IBS reacted in the same way. When common triggers for IBS (gluten, wheat, soy and cow milk) were injected into the intestine wall of 12 IBS patients, they produced localised immune reactions similar to that seen in the mice. No reaction was seen in healthy volunteers.

Boeckxstaens said that with the studies on mice, the team speculated the immune response was triggered as “a bystander response to a food antigen triggered by the infection”. He said that further in-depth immunological studies were needed to further unravel the exact mechanism initiating or driving the immune response.

Earlier work by Boeckxstaens and his colleagues has shown that blocking histamine (called mast cells), improves the condition of people with IBS and a larger clinical trial of the antihistamine treatment is currently underway.

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