Purpose of review Molecular allergology uses pure, mainly recombinant and structurally defined allergen molecules and allergen-derived epitopes to study mechanisms of IgE-associated allergy, to diagnose, and even predict the development of allergic manifestations and to treat and prevent IgE-associated allergies. Atopic dermatitis, a chronic inflammatory skin disease is almost always associated with IgE sensitization to allergens. However, also non-IgE-mediated pathomechanisms seem to be operative in atopic dermatitis and it is often difficult to identify the disease-causing allergens. Here we review recent work showing the usefulness of molecular allergology to study mechanisms of atopic dermatitis, for diagnosis and eventually for treatment and prevention of atopic dermatitis. Recent findings IgE sensitization to airborne, food-derived, microbial allergens, and autoallergens has been found to be associated with atopic dermatitis. Using defined allergen molecules and non-IgE-reactive allergen derivatives, evidence could be provided for the existence of IgE- and non-IgE-mediated mechanisms of inflammation in atopic dermatitis. Furthermore, effects of epicutaneous allergen administration on systemic allergen-specific immune responses have been studied. Multi-allergen tests containing micro-arrayed allergen molecules have been shown to be useful for the identification of culprit allergens in atopic dermatitis and may improve the management of atopic dermatitis by allergen-specific immunotherapy, allergen avoidance, and IgE-targeting therapies in a personalized medicine approach. Summary Molecular allergology allows for dissection of the pathomechanisms of atopic dermatitis, provides new forms of allergy diagnosis for identification of disease-causing allergens, and opens the door to new forms of management by allergen-specific and T cells-targeting or IgE-targeting interventions in a personalized medicine approach.
Allergens can act as disease-triggering factors in atopic dermatitis (AD) patients. The aim of the study was to elucidate the molecular IgE sensitization profile in children with and without AD living in urban and rural areas of South Africa.Specific IgE reactivity was assessed in 166 Black South African children aged 9-38 months using a comprehensive panel of microarrayed allergens. According to clinical characterization children fell in four groups, urban AD cases (n = 32), urban controls (non-AD, n = 40), rural cases (n = 49) and rural controls (non-AD, n = 45).IgE reactivity to at least one of the allergens was detected in 94% of urban and 86% of rural AD children. House dust mite (HDM; 81% urban, 74% rural AD) and animal-derived allergens (50% urban, 31% rural AD) were the most frequently recognized respiratory allergens, whereas IgE to pollen allergens was almost absent. Urban AD children showed significantly higher frequency of IgE reactivity (50%) to mouse lipocalin, Mus m 1, than rural AD children (12%). The most frequently recognized food allergens were from egg (63% urban, 43% rural AD), peanut (31% vs 41%), and soybean (22% vs 27%), whereas milk sensitization was rare. α-gal-specific IgE almost exclusively occurred in rural children (AD: 14%, non-AD: 49%).Molecular allergy diagnosis detects frequent IgE sensitization to HDM, animal but not pollen allergens and to egg, peanut, and soy, but not milk allergens in African AD children. Urban AD children reacted more often to Mus m 1, whereas α-gal sensitization is more common in rural children likely due to parasite exposure.
Background: IgE-reactivity to antigens from gram-positive and negative bacteria is common in patients suffering from respiratory and skin manifestations of allergy, but the routes and mechanisms of sensitisation are not fully understood. The analysis of the genome, transcriptome and microbiome of house dust mites has shown that Staphylococcus aureus and Escherichia coli species are abundant bacteria within the house dust mites microbiome. Therefore, our aim was to investigate if house dust mites are carriers of bacterial antigens leading to IgE sensitisation in patients suffering from atopic dermatitis.Methods: Plasma samples from atopic dermatitis patients (n = 179) were analysed for IgE-reactivity to a comprehensive panel of micro-arrayed house dust mites allergen molecules and to Staphylococcus aureus and Escherichia coli by IgE immunoblotting. Antibodies specific for Staphylococcus aureus and Escherichia coli antigens were tested for reactivity to nitrocellulose-blotted extract from purified house dust mites bodies and the IgE-reactive antigens were detected by IgE-immunoblot inhibition experiments. IgE antibodies directed to bacterial antigens in house dust mites were quantified by IgE ImmunoCAPTM inhibition experiments.Results: IgE-reactivity to bacterial antigens was significantly more frequent in atopic dermatitis patients sensitised to house dust mites than in atopic dermatitis patients without house dust mites sensitisation. Staphylococcus aureus and Escherichia coli antigens were detected in immune-blotted house dust mites extract and the presence of IgE-reactive antigens in house dust mites was demonstrated by qualitative and quantitative IgE inhibition experiments.Conclusions: House dust mites may serve as carriers of bacteria responsible for the induction of IgE sensitisation to microbial antigens.
Abstract Background IgE reactivity to antigens from Gram‐positive and Gram‐negative bacteria is common in patients suffering from respiratory and skin manifestations of allergy, but the routes and mechanisms of sensitization are not fully understood. The analysis of the genome, transcriptome and microbiome of house dust mites ( HDM ) has shown that Staphylococcus aureus ( S. aureus ) and Escherichia coli ( E. coli ) species are abundant bacteria within the HDM microbiome. Therefore, our aim was to investigate whether HDM are carriers of bacterial antigens leading to IgE sensitization in patients suffering from atopic dermatitis. Methods Plasma samples from patients with AD (n = 179) were analysed for IgE reactivity to a comprehensive panel of microarrayed HDM allergen molecules and to S. aureus and E. coli by IgE immunoblotting. Antibodies specific for S. aureus and E. coli antigens were tested for reactivity to nitrocellulose‐blotted extract from purified HDM bodies, and the IgE‐reactive antigens were detected by IgE immunoblot inhibition experiments. IgE antibodies directed to bacterial antigens in HDM were quantified by IgE Immuno CAP ™ inhibition experiments. Results IgE reactivity to bacterial antigens was significantly more frequent in patients with AD sensitized to HDM than in AD patients without HDM sensitization. S. aureus and E. coli antigens were detected in immune‐blotted HDM extract, and the presence of IgE‐reactive antigens in HDM was demonstrated by qualitative and quantitative IgE inhibition experiments. Conclusion House dust mites ( HDM ) may serve as carriers of bacteria responsible for the induction of IgE sensitization to microbial antigens.
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