Centre for Human Drug Research, Leiden, The Netherlands.
Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands.
Exp Dermatol. 2024 Jan;33(1):e14952. doi: 10.1111/exd.14952. Epub 2023 Nov 16.
Seborrheic dermatitis (SD) is a chronic inflammatory skin disease characterized by erythematous papulosquamous lesions in sebum rich areas such as the face and scalp. Its pathogenesis appears multifactorial with a disbalanced immune system, Malassezia driven microbial involvement and skin barrier perturbations. Microbial involvement has been well described in SD, but skin barrier involvement remains to be properly elucidated. To determine whether barrier impairment is a critical factor of inflammation in SD alongside microbial dysbiosis, a cross-sectional study was performed in 37 patients with mild-to-moderate facial SD. Their lesional and non-lesional skin was comprehensively and non-invasively assessed with standardized 2D-photography, optical coherence tomography (OCT), microbial profiling including Malassezia species identification, functional skin barrier assessments and ceramide profiling. The presence of inflammation was established through significant increases in erythema, epidermal thickness, vascularization and superficial roughness in lesional skin compared to non-lesional skin. Lesional skin showed a perturbed skin barrier with an underlying skewed ceramide subclass composition, impaired chain elongation and increased chain unsaturation. Changes in ceramide composition correlated with barrier impairment indicating interdependency of the functional barrier and ceramide composition. Lesional skin showed significantly increased Staphylococcus and decreased Cutibacterium abundances but similar Malassezia abundances and mycobial composition compared to non-lesional skin. Principal component analysis highlighted barrier properties as main discriminating features. To conclude, SD is associated with skin barrier dysfunction and changes in the ceramide composition. No significant differences in the abundance of Malassezia were observed. Restoring the cutaneous barrier might be a valid therapeutic approach in the treatment of facial SD.
脂溢性皮炎（SD）是一种慢性炎症性皮肤病，其特征是皮脂丰富区域（如面部和头皮）出现红斑丘疹鳞屑病变。其发病机制似乎是多因素的，包括免疫系统失衡、马拉色菌驱动的微生物参与和皮肤屏障紊乱。SD 中的微生物参与已得到充分描述，但皮肤屏障的参与仍有待充分阐明。为了确定在 SD 中，微生物失调的同时，屏障损伤是否是炎症的关键因素，对 37 例轻度至中度面部 SD 患者进行了横断面研究。他们的病变和非病变皮肤通过标准化的 2D 摄影、光学相干断层扫描（OCT）、包括马拉色菌鉴定在内的微生物分析、功能皮肤屏障评估和神经酰胺分析进行全面和非侵入性评估。通过与非病变皮肤相比，病变皮肤中红斑、表皮厚度、血管化和表面粗糙度的显著增加，确定了炎症的存在。病变皮肤的皮肤屏障受到干扰，其神经酰胺亚类组成存在潜在偏斜，链延长受损，链不饱和增加。神经酰胺组成的变化与屏障损伤相关，表明功能屏障和神经酰胺组成之间存在相互依存关系。与非病变皮肤相比，病变皮肤的金黄色葡萄球菌和减少的 Cutibacterium 丰度显著增加，但马拉色菌丰度和真菌组成相似。主成分分析强调了屏障特性是主要的区分特征。总之，SD 与皮肤屏障功能障碍和神经酰胺组成的变化有关。未观察到马拉色菌丰度的显著差异。恢复皮肤屏障可能是治疗面部 SD 的有效治疗方法。
