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The aryl hydrocarbon receptor AhR links atopic dermatitis and air pollution via induction of the neurotrophic factor artemin
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The aryl hydrocarbon receptor AhR links atopic dermatitis and air pollution via induction of the neurotrophic factor artemin
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Journal Article
The aryl hydrocarbon receptor AhR links atopic dermatitis and air pollution via induction of the neurotrophic factor artemin
2017
Overview
There are suspected links between air pollution and atopic dermatitis, but the mechanism has remained unclear. Yamamoto and colleagues demonstrate that air pollutants trigger activation of the aryl hydrocarbon receptor in the skin, hyperinnervation and an itch-scratch cycle that leads to atopic dermatitis.
Atopic dermatitis is increasing worldwide in correlation with air pollution. Various organic components of pollutants activate the transcription factor AhR (aryl hydrocarbon receptor). Through the use of AhR-CA mice, whose keratinocytes express constitutively active AhR and that develop atopic-dermatitis-like phenotypes, we identified
Artn
as a keratinocyte-specific AhR target gene whose product (the neurotrophic factor artemin) was responsible for epidermal hyper-innervation that led to hypersensitivity to pruritus. The activation of AhR via air pollutants induced expression of artemin, alloknesis, epidermal hyper-innervation and inflammation. AhR activation and
ARTN
expression were positively correlated in the epidermis of patients with atopic dermatitis. Thus, AhR in keratinocytes senses environmental stimuli and elicits an atopic-dermatitis pathology. We propose a mechanism of air-pollution-induced atopic dermatitis via activation of AhR.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ 631/337
/ Air Pollutants - adverse effects
/ Animals
/ Basic Helix-Loop-Helix Transcription Factors - genetics
/ Basic Helix-Loop-Helix Transcription Factors - metabolism
/ Dermatitis, Atopic - immunology
/ Humans
/ Mice
/ Nerve Tissue Proteins - genetics
/ Nerve Tissue Proteins - metabolism
/ Receptor, EphB2 - metabolism
/ Receptors, Aryl Hydrocarbon - genetics
