Ontology highlight
ABSTRACT:
PROVIDER: PRJNA912344 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22807221_1.fastq.gz | Fastqsanger.gz | |||
| SRR22807221_2.fastq.gz | Fastqsanger.gz | |||
| SRR22807222_1.fastq.gz | Fastqsanger.gz | |||
| SRR22807222_2.fastq.gz | Fastqsanger.gz | |||
| SRR22807223_1.fastq.gz | Fastqsanger.gz |
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Project description:Low environmental humidity aggravates symptoms of inflammatory skin diseases, e.g. of Atopic Dermatitis (AD). Using mice that develop AD-like symptoms, we show that an increase in environmental humidity rapidly rescues their cutaneous inflammation and associated epidermal abnormalities. Quantitative proteomics analysis of epidermal lysates of mice kept at low or high humidity identified novel humidity-regulated proteins, including Clca2/Clca3a2, a protein with previously unknown function in the skin.
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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.
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