孕妇X受体可降低亚托皮肤炎中颗粒物诱导的17型炎症
Ji Su Lee1,2, Youngae Lee2,3,4, Sunhyae Jang2,4,5
1Department of Dermatology, Seoul National University College of Medicine, Seoul, Republic of Korea.
Frontiers in immunology
|October 14, 2024
概括
颗粒物 (PM) 暴露会通过诱导17型炎症使亚托皮炎 (AD) 恶化. 孕妇X受体 (PXR) 激活通过抑制NF-κB通路来减轻这种炎症,这表明PXR是PM诱导AD的治疗标.
科学领域:
- 环境健康 环境健康
- 皮肤病学 皮肤病学
- 免疫学 免疫学 免疫学
背景情况:
- 流行病学研究将颗粒物暴露与阿托皮性皮肤炎 (AD) 恶化联系起来.
- 导致PM引起的AD的确切机制尚不清楚.
- 孕妇X受体 (PXR) 已成为与AD相关的皮肤炎症的潜在因素.
研究的目的:
- 调查颗粒物暴露对AD的影响.
- 阐明PXR在PM诱导的AD病变发生中的作用.
主要方法:
- 在体内和体外使用类似AD的模型,包括BALB/c小鼠,HaCaT细胞和小鼠CD4T细胞.
- 评估了皮肤炎得分,皮肤厚度和炎症媒介水平 (IL-17A,IL-23A,IL-1β,IL-6).
- 检查了PXR信号通路,包括Rifampicin的PXR敲除和激活,以及它对NF-κB通路的影响.
主要成果:
- 在AD模型中,暴露于PM显著恶化了皮肤炎和皮肤厚度.
- 在小鼠和人类皮肤细胞中,PM增加了17型炎症媒介.
- 里芬素的PXR激活减少了PM诱导的炎症,而PXR倒置加剧了炎症.
- 发现PXR激活可以抑制NF-κB信号通路.
结论:
- 在AD中,暴露于PM会触发17型炎症和PXR激活.
- PXR激活通过抑制NF-κB通路来改善PM诱导的17型炎症.
- PXR是管理PM加重AD的潜在治疗标.
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