Researchers at Tulane University have identified a novel approach for treating eosinophilic esophagitis (EoE), a chronic immune system disease that can cause children to struggle with eating due to complications with swallowing.
EoE is a condition in which food or airborne allergens trigger an accumulation of a particular type of white blood cell, eosinophils, in the esophagus.
This accumulation leads to a thickening and shortening of the esophagus, causing difficulty swallowing and even instances where food becomes lodged in the throat.
The disease, which occurs in about one in 1,500 children and one in 2,000 adults, can lead to malnutrition, weight loss, and stunted growth in children due to feeding difficulties.
Published in Nature’s Communications Biology journal, the study identified that EoE is caused by a protein called Interleukin-18 (IL-18), which is involved in the body’s immune response and can cause inflammation when produced in excess.
The researchers discovered that blocking a pathway known as the NLRP3 pathway, which leads to the release of IL-18, could prevent the onset of EoE, even when induced by food or airborne allergens.
According to Dr. Anil Mishra, the lead author of the study and director of the Eosinophilic Disorder Center at the Tulane University School of Medicine, this discovery could prove to be game-changing in the treatment of EoE, a disease often misdiagnosed as gastrointestinal reflux disease (GERD).
One drug, known as VX-765, was identified as a potential treatment for humans suffering from EoE.
Crucially, this drug would only target the pathogenic eosinophils produced by IL-18 and would not interfere with white blood cells produced by IL-5, a protein necessary for innate immunity.
Dr. Mishra suggests that a clinical trial would be the next step towards validating this treatment’s effectiveness.
This groundbreaking study offers hope for the many children and adults suffering from EoE and could provide a more targeted and effective treatment for this challenging condition.
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The study was published in Communications Biology.
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