Department of Pharmacology and Toxicology, School of Biomedical Sciences, University of Otago, Dunedin 9054, New Zealand.
The New Zealand Institute for Plant and Food Research Limited, Nelson 7043, New Zealand.
Int J Mol Sci. 2023 Nov 16;24(22):16383. doi: 10.3390/ijms242216383.
Atopic dermatitis is a chronic condition where epidermal barrier dysfunction and cytokine production by infiltrating immune cells exacerbate skin inflammation and damage. A total lipid extract from , a brown seaweed, was previously reported to suppress inflammatory responses in monocytes. Here, treatment of human HaCaT keratinocytes with lipids inhibited tumour necrosis factor (TNF)-α induced TNF receptor-associated factor 2 and monocyte chemoattractant protein (MCP)-1 protein production. HaCaT cells stimulated with TNF-α, interleukin (IL)-4, and IL-13 showed loss of claudin-1 tight junctions, but little improvement was observed following lipid pre-treatment. Three-dimensional cultures of HaCaT cells differentiated at the air-liquid interface showed increased MCP-1 production, loss of claudin-1 tight junctions, and trans-epidermal leakage with TNF-α, IL-4, and IL-13 stimulation, with all parameters reduced by lipid pre-treatment. These findings suggest that lipids have anti-inflammatory and barrier-protective effects on keratinocytes, which may be beneficial for the treatment of atopic dermatitis or other skin conditions.
特应性皮炎是一种慢性疾病,表皮屏障功能障碍和浸润免疫细胞产生的细胞因子会加剧皮肤炎症和损伤。先前有报道称,一种褐藻的总脂质提取物可抑制单核细胞中的炎症反应。在这里,用 脂质处理人 HaCaT 角质形成细胞可抑制肿瘤坏死因子 (TNF)-α诱导的 TNF 受体相关因子 2 和单核细胞趋化蛋白 (MCP)-1 蛋白的产生。用 TNF-α、白细胞介素 (IL)-4 和 IL-13 刺激的 HaCaT 细胞失去了紧密连接蛋白-1 (claudin-1) 紧密连接,但脂质预处理后观察到的改善很小。在气液界面分化的 HaCaT 细胞的三维培养物中,随着 TNF-α、IL-4 和 IL-13 的刺激,MCP-1 的产生增加,claudin-1 紧密连接蛋白丢失,出现经表皮渗漏,所有参数均通过脂质预处理降低。这些发现表明, 脂质对角质形成细胞具有抗炎和屏障保护作用,这可能有益于特应性皮炎或其他皮肤状况的治疗。