Homo sapiens
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ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-36842
PROVIDER: PRJNA157271 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcription profiling by array of acute and chronic atopic dermatitis compared to normal skin
2025-01-24 | E-GEOD-36842 | ExpressionAtlas
Project description:Atopic dermatitis (AD) is a common disease, with an increasing prevalence. The primary pathogenesis of the disease is still elusive, resulting in lack of specific treatments. The prevailing view is that AD is a biphasic, T-cell polarized disease, with Th2 predominating acute AD, and a switch to Th1 characterizing chronic disease. Identification of factors that participate in onset of lesions and maintenance of chronic lesions is critical for development of targeted therapeutics. We performed global genomic, molecular and cellular profiling of paired non-lesional, acute, and chronic skin biopsies from ten AD patients. Onset of acute lesions is associated with a striking increase in a subset of terminal differentiation proteins, specifically the IL-22-modulated S100A7-9. Correspondingly, acute disease is associated with significant increases in gene expression levels of the major Th22- (IL-22) and Th2- (IL-4, IL-31) cytokines and Th17-regulated genes (CCL20, PI3/Elafin), without significant changes in IL-17. A lesser induction of Th1- (IFNγ, MX-1, CXCL9-11) associated genes was detected in acute disease. Chronic skin lesions are characterized by significantly intensified activation of Th22, Th2 and Th1. Our data establish increased expression of S100A7-9 and other epidermal genes at onset of acute AD, with parallel activation of Th2 and Th22 cytokines. Our findings suggest an absence of switch mechanism in chronic disease and instead indicate that progression to chronic lesions is associated with intensified activation of immune axes that initiate onset of acute lesions, particularly Th22 and Th2. This alters the prevailing view of pathogenesis, with important therapeutic implications. Acute, chronic, and non-lesional skin samples were collected from ten patients with moderate-to-severe AD that met our inclusion criteria, under an institutional review board–approved protocol. The following criteria were employed to define acute AD and distinguish true acute from “acute on chronic” skin lesions: a) new lesions of <72 hours duration, as previously defined;14 b) lack of skin lichenification; c) lack of regenerative hyperplasia, as defined by epidermal thickness ≤150μ [hematoxylin and eosin (H&E)] and basal or confluent supra-basal Keratin 16 (K16) positivity. No systemic or topical treatments were allowed for ≥4 weeks prior to biopsies. Biopsy specimens were frozen in optimal cutting temperature (OCT) for immunohistochemistry (IHC) and liquid nitrogen for RNA extraction.
2012-09-21 | E-GEOD-36842 | biostudies-arrayexpress
Project description:Atopic dermatitis (AD) is a common disease, with an increasing prevalence. The primary pathogenesis of the disease is still elusive, resulting in lack of specific treatments. The prevailing view is that AD is a biphasic, T-cell polarized disease, with Th2 predominating acute AD, and a switch to Th1 characterizing chronic disease. Identification of factors that participate in onset of lesions and maintenance of chronic lesions is critical for development of targeted therapeutics. We performed global genomic, molecular and cellular profiling of paired non-lesional, acute, and chronic skin biopsies from ten AD patients. Onset of acute lesions is associated with a striking increase in a subset of terminal differentiation proteins, specifically the IL-22-modulated S100A7-9. Correspondingly, acute disease is associated with significant increases in gene expression levels of the major Th22- (IL-22) and Th2- (IL-4, IL-31) cytokines and Th17-regulated genes (CCL20, PI3/Elafin), without significant changes in IL-17. A lesser induction of Th1- (IFNγ, MX-1, CXCL9-11) associated genes was detected in acute disease. Chronic skin lesions are characterized by significantly intensified activation of Th22, Th2 and Th1. Our data establish increased expression of S100A7-9 and other epidermal genes at onset of acute AD, with parallel activation of Th2 and Th22 cytokines. Our findings suggest an absence of switch mechanism in chronic disease and instead indicate that progression to chronic lesions is associated with intensified activation of immune axes that initiate onset of acute lesions, particularly Th22 and Th2. This alters the prevailing view of pathogenesis, with important therapeutic implications.
2012-09-21 | GSE36842 | GEO
Project description:House dust mite/HDM atopy patch test/APT elicits positive reactions in the majority of atopic dermatitis/AD and healthy individuals. Experimental systems for new-onset/chronic AD are needed to support rapid therapeutic development, particularly since animal models representing AD pathology in humans are lacking. HDM APT historically simulated AD, but its suitability to model the emerging AD skin phenotype as Th2/Th22 polarized with Th1 and Th17 components is unknown. To assess whether HDM APT tissues reproduce acute or chronic AD, positive HDM APT (n=14) were compared with nonlesional, acute (<72hrs; n=10), and chronic phase AD biopsies (n=8), allergic contact reactions (to nickel [n=10] and fragrance [n=3]) using arrays.
2018-09-25 | GSE95759 | GEO
Project description:Atopic dermatitis epidermis PCT-DIA
2024-06-05 | E-PROT-145 | ExpressionAtlas
Project description:Atopic dermatitis (AD) is the most common inflammatory skin disease. Stat3 mutation is a major cause of hyper IgE syndrome (HIES), which consistently represent AD like eczematous dermatitis. Based on multi-dimensional transcriptome analysis in pre- and post-flares skin, dermatitis phenotype was controlled by sequential two steps of Stat3 deficiency and environmental pathogenic stimuli. The Stat3 deficiency determined the barrier integrity that lowered threshold of inflammation, but this step was not sufficient to form pathogenicity. Transcriptome data indicated that emergence of dermatitis phenotype need to trigger robust activation of NFB pathway and TH2 cells. Continuous colonization of Staphylococcus aureus was an environmental stimulus to lower the activation threshold of TH2 inflammation in the skin.
2021-10-12 | GSE185340 | GEO
Project description:Atopic dermatitis (AD) is the chronic inflammatory skin disease accompanied with severe pruritus. To explore the roles of EGR1 in atopic dermatitis and the relationship between EGR1 and pruritus-scratching behavior, we used a atopic dermatitis-like mouse model driven by house dust mite (HDM) treatment in wild type and EGR1 KO mice, followed with RNA-sequencing analysis.
2024-01-15 | GSE214750 | GEO
Project description:Early Activation of Th2 Inflammatory and Pruritogenic Pathways in Acute Canine Atopic Dermatitis Skin Lesions
| PRJNA299152 | ENA
Project description: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.
2009-10-31 | E-GEOD-16161 | biostudies-arrayexpress
Project description:TSLP is believed to play a role in allergic diseases such as atopic dermatitis and asthma, through its activation of dendritic cells which later promote the induction of inflammatory Th2 cells. We sought to characterize the inflammatory response induced by TSLP challenge in naive and OVA-sensitized mice using gene expression profiling.
2015-10-11 | GSE41667 | GEO