Louisiana [US], August 6 : Researchers have discovered a new treatment for chronic immune system disease that can prevent children from eating.
Food allergies or airborne allergens cause eosinophils, a type of white blood cell, to accumulate in the lining of the oesophagus, causing eosinophilic esophagitis (EoE). This shortens the oesophagus and thickens the oesophagal wall, making swallowing difficult and causing food to become stuck in the throat.
The disease affects approximately one in every 2,000 adults, but it is more common in children (1 in every 1,500), where symptoms can be more difficult to diagnose and pose greater risks, as difficulty feeding can lead to malnutrition, weight loss, and poor growth.
The new study, published in Nature Communications Biology, discovered that the disease is caused by Interleukin-18 (IL-18), a protein involved in the innate immune response that, when produced in excess, can cause inflammation.
When a food allergen enters the body, it activates a pathway that regulates the innate immune system, causing the release of proinflammatory proteins such as IL-18. This results in the production of eosinophils, which cause esophageal damage.
The study discovered that inhibiting this pathway, known as the NLRP3 pathway, and the release of IL-18 successfully prevented the development of EoE from both food and airborne allergens.
“Parents and doctors may not be aware of this, but this is a very prominent and serious disease in the pediatric population, and it is increasing in number because it is directly related to food allergens, which are also on the rise,” said lead author Dr. Anil Mishra, director of the Eosinophilic Disorder Center at the Tulane University School of Medicine.
“In this study, we show that after treating the disease in animals, the disease is gone and completely in remission."
The findings are crucial for a disease that was not identified until the 1990s. For many years, EoE was misdiagnosed as gastrointestinal reflux disease (GERD), despite GERD medication being ineffective in treating EoE.
Additionally, this study’s findings replace decades of thinking that Th2 cells play a major role in triggering EoE.
“Given the paucity of mechanistic information and treatment strategies for EoE, we feel the proposed studies are highly relevant and are poised to have a major impact on establishing the significance of NLRP3-IL-18 pathway in the initiation of EoE pathogenesis,” Mishra said.
The study identified one existing drug, VX-765, as an inhibitor that may work as a treatment for humans. Importantly, this inhibitor would only deplete pathogenic eosinophils generated and transformed by IL-18 and not affect white blood cells created by IL-5, a protein important for maintaining innate immunity.
Mishra said a clinical trial would be the next step to determining the treatment’s effectiveness.
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