Scientists have found the cause of a chronic inflammatory
disorder of the esophagus, paving the way for new therapeutic strategies
for an enigmatic and hard-to-treat food allergy.
Researchers have identified a novel genetic and molecular pathway in the esophagus that causes eosinophillic esophagitis (EoE).
EoE is triggered by allergic hypersensitivity to certain foods
and an over-accumulation in the esophagus of white blood cells called
eosinophils (part of the body's immune system).
EoE can cause a variety of gastrointestinal complaints including
reflux-like symptoms, vomiting, difficulty swallowing, tissue scarring,
fibrosis, the formation of strictures and other medical complications.
The multi-institutional team of researchers led by scientists at
Cincinnati Children's Hospital Medical Center identified a molecular
pathway specific to epithelial tissue in the esophagus involving a gene
called CAPN14, which they found becomes dramatically up-regulated in the
disease process.
Epithelial cells help form the membrane of the esophagus. The
scientists reported that when these cells were exposed to a well-known
molecular activator of EoE - an immune hormone called Interleukin 13
(IL-13) - it caused dramatic up-regulation of CAPN14.
The researchers said this happened in what they described as an epigenetic hotspot for EoE on the cells' chromosomes.
CAPN14 encodes an enzyme in the esophagus that is part of the
disease process called calpain14, according to Marc E Rothenberg, senior
investigator on the study and director of the Center for Eosinophilic
Disorders at Cincinnati Children's.
The findings open a new way to consider therapeutic options
because calpain14 is an enzyme that can be inhibited by drugs, which
means it may be possible to modify the expression and activity of
calpain14.
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