Intra-individual genome expression analysis reveals a specific molecular signature of psoriasis and eczema
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ABSTRACT: Comparing molecular signatures of psoriasis and eczema in patients co-affected by both diseases provides a comprehensive understanding of disease pathogenesis as well as a diagnostic tool to differentiate these widespread inflammatory skin diseases. In patients affected by both psoriasis and non-atopic or atopic eczema simultaneously (n=24), whole genome expression arrays of psoriasis, eczema, and non-involved skin were performed Arrays MQ_35 and MQ_41 did not pass quality control and thus were not normalized and were excluded from this Series.
Project description:Comparing molecular signatures of psoriasis and eczema in patients co-affected by both diseases provides a comprehensive understanding of disease pathogenesis as well as a diagnostic tool to differentiate these widespread inflammatory skin diseases.
Project description:Characteization host-microbiome interactions in patients with allergic (model: atopic dermatitis) and autoimmune (model: psoriasis) diseases by integration of microarray transcriptome data with 16S microbial profiling. 6mm punch biopsies were collected from the skin of atopic dermatitis and psoriasis patients alongside healthy volunteers, and subjected to analysis using Affymetrix Human Gene ST 2.1 arrays.
Project description:Biologics targeting the tumour necrosis factor (TNF) and interleukin (IL)-17/23 axis are highly effective treatments for psoriasis but can result in cutaneous adverse events. The pathogenesis of paradoxical eczema, the occurrence of an atopic dermatitis phenotype after biologic initiation in people with psoriasis, is unknown. Using single cell RNA-seq and mass cytometry, we found increased expression of TNF, interferon (IFN)-γ and IFN-α and their signalling pathways in paradoxical eczema case cell clusters compared with matched psoriasis controls. Genetic variants influencing expression of TNF pathway genes were associated with paradoxical eczema in a separate genotyped cohort, and this association was independent of known atopic risk loci. This suggests that paradoxical eczema has a predominantly type 1 systemic inflammatory signature, and that genetic susceptibility to aberrant TNF pathway signalling could contribute to development of this phenotype during biologic treatment.
Project description:Anti-TNF-alpha therapy has made a significant impact on the treatment of psoriasis. Despite being designed to neutralize TNF-alpha activity, the mechanism of action of these agents in the resolution of psoriasis remains unclear. The aim of this study was to better understand the mechanism of action of etanercept by examining very early changes in the lesional skin of psoriasis patients. 20 chronic plaque psoriasis patients were enrolled and received 50mg etanercept twice weekly. Skin biopsies were obtained before treatment and on days 1, 3, 7 and 14 post-treatment. Skin mRNA expression was analysed by microarray. Twenty individuals with chronic plaque psoriasis were enrolled (age range 18-75 years). Entry criteria included age greater than 18 years and stable plaque-type psoriasis involving at least 10% body surface area. Exclusion criteria included use of systemic psoriasis therapy within 4 weeks, topical therapy within 2 weeks, or severe co-morbid diseases. For 12 weeks, subjects received etanercept (Enbrel) 50mg twice a week subcutaneously. At baseline, 6 mm punch biopsies were obtained under local anaesthesia (lidocaine) from uninvolved skin and a target plaque. Subsequent biopsies were taken on days 1, 3, 7 and 14 of therapy from the same target plaque.
Project description:This study includes RNAseq data of lesional and autologous non-lesional skin from patients with non-communicable inflammatory skin diseases, including psoriasis, nummular eczema and atopic dermatitis.
Project description:The aim of this study was to find disease-associated genes in atopic eczema. Experiment Overall Design: Skin biopsies were analyzed from ten patients with active atopic eczema and ten healthy controls.
Project description:Psoriasis is a chronic inflammatory skin disease characterized by marked proliferation of keratinocytes leading to pronounced epidermal hyperplasia, elongation of rete ridges and hyperkeratosis. The most common form of psoriasis, chronic plaque psoriasis (Psoriasis vulgaris), involves relatively stable occurrence and progression of sharply demarcated lesions, usually on the trunk and extremities, which share a combination of trademark histological features, including tortuous and dilated dermal capillaries, loss of the epidermal granular layer, and accumulation of neutrophils beneath parakeratotic scale. In this study, whole-genome transcriptional profiling was used to characterize gene expression in 4 lesional and uninvolved skin samples obtained from patients with stable chronic plaque psoriasis. Skin mRNA expression was analysed by microarray. Four individuals with chronic plaque psoriasis were enrolled. 6 mm punch biopsies were obtained under local anaesthesia (lidocaine) from uninvolved skin and a target plaque.
Project description:We analyzed m6A modifications in skin lesions of patients with psoriasis or atopic dermatitis (AD). The results of this study will help to gain insight into the molecular basis of m6A modification in inflammatory skin diseases such as psoriasis or atopic dermatitis.