脂质体
脂类学
特应性皮炎
斯科拉德
睑板腺
转录组
皮脂腺
内根鞘
内科学
脂质代谢
鞘脂
医学
内分泌学
皮肤病科
疾病
免疫学
毛囊
化学
外根鞘
基因表达
生物化学
基因
皮肤科生活质量指数
外科
眼睑
作者
H. Yin,Zhuoqiong Qiu,Ronghui Zhu,Shangshang Wang,Chaoying Gu,Xu Yao,Wei Li
出处
期刊:Allergy
[Wiley]
日期:2022-10-29
卷期号:78 (6): 1524-1537
被引量:22
摘要
Abstract Background Lipids are the major components of skin barrier, mainly produced by keratinocytes and sebaceous glands. Previous studies on barrier dysfunction of atopic dermatitis (AD) mainly focus on the lipids from keratinocytes, whereas the role of sebaceous gland‐derived lipids in AD has long been underrecognized. Methods The sebum secreted on the skin surface of AD patients was measured using the Delfin Sebum Scale. Sebum was collected using Sebutape patches and subjected for liquid chromatography tandem‐mass spectrometry (LC–MS/MS) analysis. Multivariate data analysis was applied to explore the relationship among the lipidome, clinical features, and sebaceous gland‐related molecules. Results The amount of sebum secreted from sebaceous glands was decreased in AD patients and was negatively correlated with the barrier function and disease severity. LC–MS/MS revealed the lipidome of sebum, which clustered distinctly between AD patients and healthy individuals. Among the differential lipid subclasses, triglycerides (TG) were exclusively decreased in AD patients and correlated with disease severity. The first principal component scores of AD patients, which represented the main signature of the lipidome, were positively correlated with the SCORAD scores and were significantly different across the patient groups with differential clinical symptoms such as skin dryness and pruritus. Further analysis on the previously published transcriptome data revealed aberrant expression of lipid metabolism‐related genes in non‐lesional skin of AD patients, which was associated with skin inflammation and barrier dysfunction and mainly derived from inner root sheath keratinocytes and sebaceous gland cells. Conclusion Atopic dermatitis patients demonstrated a deviated lipidome of sebum and aberrant lipid metabolism in sebaceous glands, indicating a possible role of lipids from sebaceous glands in the pathogenesis of AD.
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