Centre for Dermatology Research, Division of Musculoskeletal and Dermatological Sciences, School of Biological Sciences, The University of Manchester and Salford Royal NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK.
Lydia Becker Institute of Immunology and Inflammation and Manchester Collaborative Centre for Inflammation Research, School of Biological Sciences, Faculty of Biology Medicine and Health, University of Manchester, Manchester, UK.
Br J Dermatol. 2024 Oct 17;191(5):746-759. doi: 10.1093/bjd/ljae226.
Sex hormone changes during menopausal transition contribute to declining skin health. However, how menopause and its treatment by hormone replacement therapy (HRT) impact the skin barrier and immune system is unclear.
To examine how menopause and HRT affect the skin barrier and immune cell composition in postmenopausal women following irritant challenge.
Two cohorts of postmenopausal women were recruited to the study. The first cohort consisted of 10 untreated women [HRT-; mean (SEM) age 56.5 (1.6) years (range 48-63)] and the second was composed of 8 women receiving HRT [HRT+; mean (SEM) age 54.0 (2.1) years (range 48-63)]. Skin irritation was induced by applying topical sodium lauryl sulfate (SLS) 1.25% to occluded buttock skin for 48 h. Clinical assessment was conducted after 24 h, followed by biopsy of both SLS-challenged and unchallenged skin for analysis of skin barrier proteins and immune cell distribution using immunofluorescence.
Clinically, there were no significant differences in skin irritant responses between those taking or not taking HRT (including increased skin redness and blood flow). In response to SLS challenge a significant increase in transepidermal water loss (P < 0.05), filaggrin deposition and cytokeratin 10 (K10)+ cell layers (P < 0.01) was observed in individuals receiving HRT compared with the HRT- group. Following SLS challenge in individuals taking HRT, a significant (P < 0.01) reduction in CD207+ cells in the epidermis was observed, accompanied by an increase of CD207+ cells in the dermis, indicative of migrating Langerhans cells (LCs). Significantly fewer migrating LCs were found in those who were not receiving HRT (P < 0.01). Furthermore, the numbers of dermal dendritic cells (DCs), macrophages, and CD11c+CD206- and CD68+CD206- subsets were found to be significantly (P < 0.05) higher in those taking HRT following SLS challenge.
Individuals receiving HRT displayed enhanced skin barrier response to SLS challenge with thicker filaggrin and increased K10+ epidermal cell layers. Following challenge, HRT users exhibited elevated LC, inflammatory DC and macrophage counts in the dermis. These may render skin both more prone to inflammation and more capable of resolving it, while also promoting skin repair.
绝经期间的性激素变化会导致皮肤健康状况下降。然而，绝经及其激素替代疗法（HRT）的治疗如何影响皮肤屏障和免疫系统尚不清楚。
研究绝经和 HRT 如何影响绝经后女性在受到刺激性挑战后的皮肤屏障和免疫细胞组成。
招募了两批绝经后妇女参加这项研究。第一组包括 10 名未接受治疗的妇女[HRT-; 平均（SEM）年龄 56.5（1.6）岁（范围 48-63）]，第二组由 8 名接受 HRT 的妇女组成[HRT+; 平均（SEM）年龄 54.0（2.1）岁（范围 48-63）]。通过将 1.25%的十二烷基硫酸钠（SLS）施加到封闭的臀部皮肤上 48 小时来诱导皮肤刺激。在 24 小时后进行临床评估，然后对 SLS 挑战和未挑战的皮肤进行活检，使用免疫荧光法分析皮肤屏障蛋白和免疫细胞分布。
临床上，接受或不接受 HRT 的个体之间的皮肤刺激性反应没有显著差异（包括皮肤发红和血流量增加）。与 HRT-组相比，接受 HRT 的个体在 SLS 挑战后，表皮经皮水分流失（TEWL）（P < 0.05）、颗粒层素沉积和角蛋白 10（K10）+细胞层（P < 0.01）显著增加。在接受 HRT 的个体中，在 SLS 挑战后，表皮中的 CD207+细胞显著减少（P < 0.01），同时真皮中的 CD207+细胞增加，表明移行朗格汉斯细胞（LC）。在未接受 HRT 的个体中，发现迁移的 LC 明显减少（P < 0.01）。此外，在 SLS 挑战后，接受 HRT 的个体的真皮树突状细胞（DC）、巨噬细胞以及 CD11c+CD206-和 CD68+CD206-亚群的数量明显更高（P < 0.05）。
接受 HRT 的个体对 SLS 挑战表现出增强的皮肤屏障反应，颗粒层素和增加的 K10+表皮细胞层较厚。在受到挑战后，HRT 使用者的真皮中 LC、炎症性 DC 和巨噬细胞计数升高。这可能使皮肤更容易发生炎症，更有能力解决炎症，同时促进皮肤修复。
