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]