Atopic dermatitis (eczema)

Molecular Diagnostics of Psoriasis, Atopic Dermatitis, Allergic Contact Dermatitis and Irritant Contact Dermatitis.

Br J Dermatol. 2009 Oct 10;

Authors: Kamsteeg M, Jansen PA, van Vlijmen-Willems IM, van Erp PE, Rodijk-Olthuis D, van der Valk PG, Feuth T, Zeeuwen PL, Schalkwijk J

ABSTRACT Background: Microarray studies on the epidermal transcriptome in psoriasis and atopic dermatitis have revealed genes with disease-specific expression in keratinocytes of lesional epidermis. These genes are possible candidates for disease-specific pathogenetic changes, but could also provide a tool for molecular diagnostics of inflammatory skin conditions in general. Objectives: To analyze if gene expression signatures as found in purified epidermal cells from atopic dermatitis are also present in other eczematous conditions such as allergic and irritant contact dermatitis. Methods: We used real-time quantitative PCR, immunohistochemistry and bioinformatics to investigate gene expression in different forms of eczema. Normal epidermis and psoriatic epidermis were analyzed for comparison. Results: Carbonic anhydrase II was highly induced in epidermis from all forms of eczema but not in psoriasis. Remarkably, the presumed neuron-specific Nel-like protein 2 showed a strong induction only in atopic dermatitis epidermis. Interleukin-1F9, elafin, beta-defensin-2 and vanin-3 were strongly induced in psoriasis, but not in any type of eczema. High levels of the chemokines CCL17 and CXCL10 were predominantly found in epidermis of allergic contact dermatitis. The chemokine CXCL8 was highly expressed in psoriasis, atopic dermatitis, and allergic contact dermatitis but not in irritant contact dermatitis. Cluster analysis or multinomial logistic regression indicated that expression levels of a set of seven genes are a strong predictor of the type of inflammatory response. Conclusions: These observations contribute to molecular diagnostic criteria for inflammatory skin conditions.

PMID: 19818069 [PubMed - as supplied by publisher]