壓力會導致異位性皮膚炎惡化：頂尖期刊 Science 研究證實

本篇研究，“A sympathetic-eosinophil axis orchestrates psychological stress to exacerbate skin inflammation”，請見這裡（外部網站），期刊摘要如下：

Psychological stress is believed to exacerbate dermatitis, yet the neurobiological mechanisms linking stress to immune processes remain elusive.

We identified a subset of prodynorphin-positive (Pdyn+) noradrenergic sympathetic neurons in mice that specifically innervate hairy skin, mediating stress-induced exacerbation of skin inflammation in an eosinophil-dependent manner.

Genetic ablation of Pdyn+ sympathetic neurons or eosinophils mitigated stress-evoked worsening of inflammation in atopic dermatitis–like mice, whereas optogenetic activation of these neurons precipitated inflammation through eosinophils. Pdyn+ sympathetic neurons recruited eosinophils through the CCL11-CCR3 axis and activated them through the adrenergic receptor beta2 (Adrb2) in inflamed skin.

Our findings reveal a neuroimmunological mechanism underlying psychological stress–induced exacerbation of dermatitis, emphasizing the Pdyn+ sympathetic-eosinophil axis as a crucial interface between the brain and skin inflammation, with potential therapeutic implications.

原始論文

A sympathetic-eosinophil axis orchestrates psychological stress to exacerbate skin inflammation（外部網站）

Tian J, Cao Y, Li Y, Sun J, et al. Science. 2026;391(6791):1269-1277. doi:10.1126/science.adv5974

論文摘要（Google 翻譯）

以下為 Google 翻譯，並校正明顯錯誤，僅供參考，內容以英文原文為準。

交感神經-嗜酸性白血球軸調控心理壓力，加劇皮膚發炎

心理壓力被認為會使皮膚炎惡化，但連結壓力與免疫過程的神經生物學機制仍不清楚。

我們在小鼠中發現一群前強啡肽陽性（Pdyn+）的正腎上腺素性交感神經元，專門支配有毛皮膚，並以依賴嗜酸性白血球的方式，介導壓力引起的皮膚發炎惡化。

以基因方式剔除 Pdyn+ 交感神經元或嗜酸性白血球，可減輕類異位性皮膚炎小鼠因壓力誘發的發炎惡化；而以光遺傳學活化這些神經元，則會透過嗜酸性白血球引發發炎。Pdyn+ 交感神經元經由 CCL11-CCR3 軸招募嗜酸性白血球，並在發炎皮膚中透過 β2 腎上腺素受體（Adrb2）活化它們。

我們的發現揭示心理壓力誘發皮膚炎惡化的神經免疫機制，強調 Pdyn+ 交感神經-嗜酸性白血球軸是大腦與皮膚發炎之間的關鍵介面，具有潛在的治療意義。

異位性皮膚炎，期刊研究，請看這裡。

期刊研究整理，請見這裡。