Dataset Information

Broad defects in epidermal cornification in atopic dermatitis (AD) identified through genomic analysis

ABSTRACT: In this study we used genomic profiling to characterize differences in expression of genes related to epidermal growth/differentiation and inflammatory circuits in skin lesions of psoriasis and atopic dermatitis (AD), comparing expression values to normal skin. Skin biopsies were collected from 9 patients with chronic atopic dermatitis, 15 psoriasis patients, and 9 healthy volunteers. Keywords: Genetic-pathology Psoriasis and AD are common inflammatory skin diseases which share important features, including: 1) large infiltrates of T-cells and inflammatory dendritic cells in skin lesions, 2) immune activation with up-regulated expression of many cytokines, chemokines, and inflammatory molecules 3) marked epidermal hyperplasia in chronic diseased skin and 4) defective barrier function with increased transepidermal water loss (TEWL), which reflects underlying alterations in keratinocyte differentiation. Using genomic profiling we provide a comprehensive comparison of chronic psoriasis and AD skin lesions as compared with normal skin.

REANALYSIS of: E-GEOD-16161

ORGANISM(S): Homo sapiens

PROVIDER: E-GEOD-16161 | ExpressionAtlas | 2015-07-27

REPOSITORIES: ExpressionAtlas

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Dataset's files

Source:

			Action	DRS
	E-GEOD-16161-analysis-methods.tsv	Tabular
	E-GEOD-16161-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-16161-configuration.xml	Xml
	E-GEOD-16161-percentile-ranks.tsv	Tabular
	E-GEOD-16161.condensed-sdrf.tsv	Tabular

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Broad defects in epidermal cornification in atopic dermatitis identified through genomic analysis.

Guttman-Yassky Emma E Suárez-Fariñas Mayte M Chiricozzi Andrea A Nograles Kristine E KE Shemer Avner A Fuentes-Duculan Judilyn J Cardinale Irma I Lin Peng P Bergman Reuven R Bowcock Anne M AM Krueger James G JG

The Journal of allergy and clinical immunology 20091201 6

<h4>Background</h4>Psoriasis and atopic dermatitis (AD) are common, complex inflammatory skin diseases. Both diseases display immune infiltrates in lesions and epidermal growth/differentiation alterations associated with a defective skin barrier. An incomplete understanding of differences between these diseases makes it difficult to compare human disease pathology to animal disease models.<h4>Objective</h4>To characterize differences between these diseases in expression of genes related to epide ...[more]

PMID: 20004782

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Project description: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. We found overexpression of many antimicrobial genes in keratinocytes from psoriatic skin compared with atopic dermatitis skin. Interestingly, we observed that markers of normal differentiation and the activated/hyperproliferative 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. In general the microarray technique is used to probe a (very large) number of genes for say the deseased and the healthy state.Then gene ontology is used to detect the involved pathways.We did not set out to find a comprehensive list of genes involved in these skin deseases.We do suspect that the "path way" approach might be a bit anthropomorphic.Here we offered a different approach.We set out to investigate the evolutionary fitness changes from one local maximum , Psoriasis , to another , Atopie. Our hypothesis is that Psoriasis is at one extreme in the reaction of the evolution to invading micro organisms and Atopie at an other.So the vast chemical web called human being with numorous feedback and feed forward signals would then be tilted a bit in multidimensional Gene Space and the microarray technique would show us a glimpse of the involved genes. Keywords: Disease state analysis Overall design: Six array’s were analysed.Each array has a sample of Psoriatic epidermis in the Cy5 channel and a sample of Atopic epidermis in the Cy3 channel.In this experiment each patient was included only once.So each array was a biological replicate and variables other than gene expression was deliberately confounded.