摘要
Recently, it was shown that lesional skin of atopic dermatitis patients expresses low levels of some antimicrobial peptides, compared with psoriasis patients. Here we performed microarray analysis on mRNA from purified lesional epidermal cells of patients with chronic plaque psoriasis and chronic atopic dermatitis, to investigate whether this is a general phenomenon for host defense proteins, and how specific it is for this class of molecules. Microarray data were confirmed on a selected set of genes by quantitative PCR and at the protein level by immunohistochemistry. We found overexpression of many antimicrobial proteins in keratinocytes from psoriatic skin compared with atopic dermatitis skin. Interestingly, we observed that markers of normal differentiation and the activated/ hyper proliferative epidermal phenotype were expressed at equal levels. Chronic lesions of psoriasis and atopic dermatitis patients are remarkably similar with respect to cellular proliferation. We conclude that psoriatic epidermis expresses high levels of host defense proteins compared with atopic dermatitis epidermis, and this phenomenon appears to be specific for these proteins. It remains to be investigated whether this is caused by genetic polymorphisms in pathways leading to an epidermal antimicrobial response, or by differences in the cellular infiltrate in psoriasis compared with atopic dermatitis.
Recently, it was shown that matitis patients expresses low lesional skin of atopic derlevels of some antimicrobial peptides, compared with psoriasis patients. Here we performed mieroarray analysis on mRNA from purified lesional epidermal cells of patients with chronic plaque psoriasis and chronic atopie dermatitis, to investigate whether this is a general phenomenon for host defense proteins, and how specific it is for this class of molecules. Mieroarray data were confirmed on a selected set of genes by quantitative PCR and at the protein level by immunohistoehemistry. We found overexpression of many antimierobial proteins in keratinoeytes from psoriatic skin compared with atopie dermatitis skin. Interestingly, we observed that markers of normal differentiation and the activated/hyper proliferative epidermal phenotype were expressed at equal levels. Chronic lesions of psoriasis and atopie dermatitis patients are remarkably similar with respect to cellular proliferation. We conclude that psoriatic epidermis expresses high levels of host defense proteins compared with atopie dermatitis epidermis, and this phenomenon appears to be specific for these proteins. It remains to be investigated whether this is caused by genetic polymorphisms in pathways leading to an epidermal antimierobial response, or by differences in the cellular infiltrate in psoriasis compared with atopie dermatitis.
