Macrocystis pyrifera Lipids Reduce Cytokine-Induced Pro-Inflammatory Signalling and Barrier Dysfunction in Human Keratinocyte Models

Int J Mol Sci. 2023 Nov 16;24(22):16383. doi: 10.3390/ijms242216383.

Abstract

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 Macrocystis pyrifera, a brown seaweed, was previously reported to suppress inflammatory responses in monocytes. Here, treatment of human HaCaT keratinocytes with M. pyrifera 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 M. pyrifera lipids have anti-inflammatory and barrier-protective effects on keratinocytes, which may be beneficial for the treatment of atopic dermatitis or other skin conditions.

Keywords: Macrocystis pyrifera; atopic dermatitis; brown seaweed; chemokine; cytokine; epidermal barrier; inflammation; keratinocyte; lipid; tight junction.

MeSH terms

  • Claudin-1 / metabolism
  • Cytokines / metabolism
  • Dermatitis, Atopic* / metabolism
  • Humans
  • Interleukin-13 / metabolism
  • Interleukin-13 / pharmacology
  • Keratinocytes / metabolism
  • Lipids / pharmacology
  • Macrocystis* / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Tumor Necrosis Factor-alpha
  • Interleukin-13
  • Claudin-1
  • Lipids
  • Cytokines

Grants and funding

This research received no external funding.