IgE Sensitization Profiles Differ between Adult Patients with Severe and Moderate Atopic Dermatitis

<div><p>Background</p><p>Atopic dermatitis (AD) is a complex chronic inflammatory disease where allergens can act as specific triggering factors.</p><p>Aim</p><p>To characterize the specificities of IgE-reactivity in patients with AD to a broad panel of exogenous allergens including microbial and human antigens.</p><p>Methodology</p><p>Adult patients with AD were grouped according to the SCORAD index, into severe (n = 53) and moderate AD (n = 126). As controls 43 patients were included with seborrhoeic eczema and 97 individuals without history of allergy or skin diseases. Specific IgE reactivity was assessed in plasma using Phadiatop^®, ImmunoCap^™, micro-arrayed allergens, dot-blotted recombinant <i>Malassezia sympodialis</i> allergens, and immune-blotted microbial and human proteins.</p><p>Results</p><p>IgE reactivity was detected in 92% of patients with severe and 83% of patients with moderate AD. Sensitization to cat allergens occurred most frequently, followed by sensitization to birch pollen, grass pollen, and to the skin commensal yeast <i>M</i>. <i>sympodialis</i>. Patients with severe AD showed a significantly higher frequency of IgE reactivity to allergens like cat (rFel d 1) and house dust mite (rDer p 4 and 10), to <i>Staphylococcus aureus</i>, <i>M</i>. <i>sympodialis</i>, and to human antigens. In contrast, there were no significant differences in the frequencies of IgE reactivity to the grass pollen allergens rPhl p 1, 2, 5b, and 6 between the two AD groups. Furthermore the IgE reactivity profile of patients with severe AD was more spread towards several different allergen molecules as compared to patients with moderate AD.</p><p>Conclusion</p><p>We have revealed a hitherto unknown difference regarding the molecular sensitization profile in patients with severe and moderate AD. Molecular profiling towards allergen components may provide a basis for future investigations aiming to explore the environmental, genetic and epigenetic factors which could be responsible for the different appearance and severity of disease phenotypes in AD.</p>