Introduction
Asthma is a common chronic airway disease characterized by airway
inflammation, hyperresponsiveness, and variable airway obstruction,
which is often attributed to gene-environment interactions [1].
Epidemiologic studies have shown that sensitization to indoor allergens
is an important risk factor for the occurrence of acute attacks of
asthma[2].
The most prevalent indoor allergens include house dust mites (HDMs),
animal dander, moulds and cockroaches. Of these, HDMs, especially D.
pteronyssinus and D. farinae, are considered the major perennial indoor
allergen sources inducing allergic sensitization worldwide [3].
Environmental factors, microbiome, epithelial cells and immune cells
show a dynamic cross talk at the skin and mucosal barriers in the
development of atopic dermatitis, allergic rhinitis, eosinophilic
esophagitis and asthma.[4]
Recent trends in targeting allergic disorders are directed towards
personalized medicine approach which necessitates novel developments in
the area of disease phenotyping , endotyping, and the development and
application of reliable biomarkers.[4]
Increased intestinal permeability
due to the exposure to antigens in asthmatic patients may play a role in
susceptibility to environmental allergens.
Therefore, correction of the gut
barrier defect may be an additional novel approach for asthma
treatment.[34]
Gut mucosal barrier depends on efficient tight junctions which are
regulated by over 50 proteins. Zonulin is a 47 kDa protein that
increases the permeability of the small intestine. It has a role in the
intestinal mucosal innate immunity
and it is the only physiological protein proven to reversibly modulate
intestinal permeability. High serum levels of zonulin have been found in
several autoimmune diseases, e.g., celiac disease as a marker of
impaired intestinal barrier.[5]Chronic inflammation develops in
response to environmental stimuli, it leads to up-regulated expression
of zonulin and serum zonulin was found to be significantly associated
with presence and severity of atopic dermatitis.[6]