Inflammatory signature of atopic dermatitis from tissue and systemic levels
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA971093 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24490513.fastq.gz | Fastqsanger.gz | |||
| SRR24490471_1.fastq.gz | Fastqsanger.gz | |||
| SRR24490471_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 3 of 3 |
Similar Datasets
Project description:Lipids play a critical role in the skin as components of the epidermal barrier and as sig-naling molecules. Atopic dermatitis in dogs is associated with changes in the lipid composition of the skin, but whether these precede the onset of dermatitis or occur secondary to the dermatitis is unclear. We applied rapid lipid profiling mass spectrometry methods to skin and blood samples of dogs and determined changes following systemic treatment. Thirty control dogs and 30 atopic dogs with mild to moderate dermatitis were enrolled. Marked differences in lipid profiles were observed between control, nonlesional and lesional skin of dogs. Additionally, there were significant altera-tions in the lipid composition of the blood samples indicating systemic changes in lipid metabolism. Treatment with oclacitinib or lokivetmab resulted in a significant decrease of the disease clinical severity associated with changes in skin and blood lipids. A set of lipid features of the skin were selected as biomarkers that classified samples as control or atopic dermatitis with 95% accuracy, whereas blood lipids discriminated between control and atopic dogs with 82% accuracy. These data suggest that atopic dermatitis is a systemic disease and support the use of rapid lipid profiling to identify novel biomarkers.
2021-07-16 | MSV000087837 | MassIVE
Project description:The patho-mechanism of atopic dermatitis showing systemic involvement may be explained by Th17-related cytokines induced by FABP5 through systemic sensitization to a major allergen of a house dust mite.
2020-03-05 | GSE146352 | GEO
Project description:Clinical overlaps between psoriasis and atopic dermatitis are sometimes undiscernible, and there is no consensus whether to treat the overlap phenotype as psoriasis or atopic dermatitis. We enrolled patients diagnosed with either psoriasis or atopic dermatitis, and clinically re-stratified them into classic psoriasis, classic atopic dermatitis, and the overlap phenotype between psoriasis and atopic dermatitis. We compared gene expression profiles of lesional and nonlesional skin biopsy tissues between the three comparison groups. Global mRNA expression and T-cell subset cytokine expression in the skin of the overlap phenotype were consistent with the profiles of psoriasis and different from the profiles of atopic dermatitis. Unsupervised k-means clustering indicated that the best number of distinct clusters for the total population of the three comparison groups was two, and the two clusters of psoriasis and atopic dermatitis were differentiated by gene expression. Our study suggests that clinical overlap phenotype between psoriasis and atopic dermatitis has dominant molecular features of psoriasis, and genomic biomarkers can differentiate psoriasis and atopic dermatitis at molecular levels in patients with a spectrum of psoriasis and atopic dermatitis.
2023-06-24 | GSE182740 | GEO
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
2006-12-23 | GSE6601 | GEO
Project description:mRNA array analysis of total RNA from primary kertinocytes from three healthy controls, three atopic dermatitis patients and three psoriasis patients was carried out
2012-06-01 | E-MTAB-728 | biostudies-arrayexpress
Project description:TWEAK Upregulates atopic dermatitis related genes in human kearatinocytes
2023-11-28 | GSE214503 | GEO
Project description:Atopic Dermatitis Research Network
| PRJNA714989 | ENA
Project description:We aimed to feature Asian populations and identify potential biomarkers associated with disease severity by incorporating analyses of skin and serum using RNA-seq
2024-12-01 | GSE232127 | GEO
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.
2019-09-11 | E-MTAB-8149 | biostudies-arrayexpress
Project description:Atopic dermatitis is increasing worldwide, correlating with air pollutions. Various organic components of pollutants activate transcription factor AhR (aryl-hydrocarbon receptor). We have established AhR-CA mice, whose keratinocytes express constitutive-active AhR, and these mice developed atopic dermatitis-like frequent scratching and allergic inflammation. In this study we performed ChIP-seq analyses and identified keratinocyte-specific AhR target genes, including inflammatory cytokines Tslp and IL33, and neurotrophic factor Artemin. While AhR-CA mice exhibited epidermal hyperinnervation and alloknesis leading to hypersensitivity to pruritus, blockade of Artemin alleviated these phenotypes. AhR-CA mice showed scratching-induced barrier insufficiency and enhanced sensitization to epicutaneously-applied antigens, recapitulating human atopic dermatitis. Consistently, AhR activation and Artemin expression was detected in the epidermis of atopic dermatitis patients and keratinocytes exposed to air pollutants. Thus, AhR in keratinocytes senses the environmental stimuli and responds to them through moderating inflammation. We propose a mechanism in which air pollution induces atopic dermatitis through AhR activation.
2016-11-13 | GSE72449 | GEO