Search

This article discusses the role of the transient receptor potential vanilloid-3 (TRPV3) channel in inducing thymic interstitial lymphopoietin (TSLP) and its implications for itch pathways. The study found that TRPV3 activation regulates TSLP expression through calcium influx and the calcineurin/NFAT/NF-kB pathway. Carvacrol, a compound that activates TRPV3, was shown to increase TSLP and calcium influx, suggesting its involvement in TRPV3-mediated itch pathways. The findings provide insights into the molecular mechanisms of chronic pruritus and potential therapeutic targets for inflammatory skin diseases. [Extracted from the article]

Particulate matter (PM2.5) is an environmental pollutant causing skin inflammatory diseases via epidermal barrier damage. However, the mechanism and related gene expression induced by PM2.5 remains unclear. Our aim was to determine the effect of PM2.5 on human skin tissue ex vivo, and elucidate the mechanism of T helper 17 cell‐related inflammatory cytokine and skin barrier function. We verified the expression levels of gene in PM2.5‐treated human skin tissue using Quantseq (3′ mRNA‐Seq), and Gene Ontology (GO) terms and protein–protein interaction (PPI) networks were performed. The PM2.5 treatment significantly enhanced the expression of Th 1, 2, 17 and 22 cell‐related genes (cut‐off value: │1.2 │ > fold change and p < 0.05). Most of all, Th17 cell‐related genes are upregulated and those genes are associated with skin epidermal barrier function and Aryl hydrocarbon receptor (AhR), a xenobiotic receptor, pathway. In human keratinocyte cell lines, AhR‐regulated genes (e.g. AhRR, CYP1A1, IL6 and IL36G), Th17 cell‐related genes (e.g. IL17C) and epidermal barrier–related genes (e.g. SPRR2A and KRT71) are significantly increased after PM2.5. In the protein level, the secretion of IL‐6 and IL‐36G was increased in human skin tissue following PM2.5 treatment, and the expression of SPRR2A and KRT71 was significantly increased. PM2.5 exposure could ruin the skin epidermal barrier function via AhR‐ and Th17 cell‐related inflammatory pathway. [ABSTRACT FROM AUTHOR]

Carvacrol, a natural transient receptor potential vanilloid-3 activator, has been reported to cause pruritus in mice. This study aimed to evaluate the effects of carvacrol and various antipruritic agents in humans. A stimulation test with carvacrol, β-alanine, and histamine was performed. After application of the pruritic solutions, the skin was stimulated with pinpricks. In inhibition test A, Forsythia suspensa extract, containing forsythoside B (a transient receptor potential vanilloid-3 inhibitor), was applied by pricking prior to stimulation with pruritogens. In inhibition test B, olopatadine solution, tacrolimus ointment, and Scutellaria baicalensis root extract were applied, and carvacrol was applied to the same region. Carvacrol induces moderate pruritus in humans. The pruritus was relieved by Forsythia suspensa extract and olopatadine solution after 20 min of application and by tacrolimus ointment and Scutellaria baicalenis extract after 24 h of application. These results suggest that carvacrol is a pruritogen in humans, and that carvacrol-induced pruritus is inhibited by various antipruritic agents.