Eosinophilic esophagitis (EoE) is an allergic disorder seen
in approximately 1 out of 2000 people in the United States. Young children often present with vomiting
and failure to thrive, while older children and adults may have difficulties
swallowing, food impaction, or strictures in their esophagus. Despite increasing awareness and diagnosis,
the etiology remains unclear. Past
studies support the role of a subset of Helper T-cells, called TH2 cells, which
are also present in many other allergic diseases, including atopic dermatitis
(AD). In fact, approximately half of
patients with EoE have AD. But why is
that so?
In this month’s issue of the Journal of Allergy and Clinical
Immunology, Venturelli and colleagues investigate the role of abnormal skin barriers
in the development of EoE, and, in particular, the role of IL-33, a chemical
messenger whose levels are elevated in both EoE and AD (J Allergy Clin Immunol 2016; 138(5): 1367-1380). They also investigated the role of ST2, an IL-33
receptor found on basophils using a mouse model. They applied ovalbumin to the
mechanically injured skin of wild-type mice, and then to the skin of mice
lacking filaggrin (ft/ft), which tend to develop AD-like skin lesions. They then challenged both strains of mice with
intra-nasal ovalbumin. The esophagi of
these mice were then examined microscopically and through advanced genetic
analytic techniques.
They found that a disrupted skin barrier (by tape stripping
or a Filaggrin gene mutation) promotes the development of EoE, and that this is
mediated by IL-33, ST2, and basophils. They
also reported that patients with EoE have increased ST2 in their esophagus. Their
findings suggest that IL-33 could be a potential link between AD and EoE. This is an important step in understanding
how patients with AD and filaggrin deficiency tend to develop EoE. Just as importantly, it may prompt
development of new medications that block IL-33 or ST2, which could be
effective targets for EoE.
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