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Genetic priming of sensory neurons in mice that overexpress PAR2 enhances allergen responsiveness
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Genetic priming of sensory neurons in mice that overexpress PAR2 enhances allergen responsiveness
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Genetic priming of sensory neurons in mice that overexpress PAR2 enhances allergen responsiveness
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Journal Article
Genetic priming of sensory neurons in mice that overexpress PAR2 enhances allergen responsiveness
2021
Overview
Pruritus is a common symptom of inflammatory skin conditions, including atopic dermatitis (AD). Although primary sensory neurons that transmit pruritic signals are well-cataloged, little is known about the neuronal alterations that occur as a result of skin disruption in AD. To address this question, we examined the molecular and behavioral consequences of challenging Grhl3
PAR2/+ mice, which overexpress PAR2 in suprabasal keratinocytes, with serial topical application of the environmental allergen house dust mite (HDM). We monitored behavior and used RNA sequencing, qPCR, and in situ hybridization to evaluate gene expression in trigeminal ganglia (TG), before and after HDM. We found that neither Grhl3
PAR2/+ nor wild-type (WT) mice exhibited spontaneous scratching, and pruritogen-induced acute scratching did not differ. In contrast, HDM exacerbated scratching in Grhl3
PAR2/+ mice. Despite the absence of scratching in untreated Grhl3
PAR2/+ mice, several TG genes in thesemice were up-regulated compared to WT. HDM treatment of the Grhl3
PAR2/+ mice enhanced up-regulation of this set of genes and induced additional genes, many within the subset of TG neurons that express TRPV1. The same set of genes was upregulated in HDM-treated Grhl3
PAR2/+ mice that did not scratch, but at lesser magnitude. Finally, we recorded comparable transcriptional changes in IL31Tg mice, demonstrating that a common genetic program is induced in two AD models. Taken together, we conclude that transcriptional changes that occur in primary sensory neurons in dermatitis-susceptible animals underlie a genetic priming that not only sensitizes the animal to chronic allergens but also contributes to pruritus in atopic skin disease.
Publisher
National Academy of Sciences
Subject
