Lipid mediators derived from DHA alleviate DNCB-induced atopic dermatitis and improve the gut microbiome in BALB/c mice

Atopic dermatitis (AD) is a chronic inflammatory skin condition that primarily results from immune dysregulation. We determined the potential therapeutic benefits of lipid mediators (LM, 17S-monohydroxy DHA, resolvin D5, and protectin DX in a ratio of 3:47:50) produced by soybean lipoxygenase from DHA. The underlying molecular mechanisms involved in TNF-alpha/IFN-gamma-stimulated HaCaT cells as well as its effect in an AD mouse model induced by DNCB in BALB/c mice were examined. The results indicated that LM effectively attenuates the production of inflammatory cytokines (IL-6 and IL-1 beta) and chemokines (IL-8 and MCP-1) by inhibiting the NF-kappa B signaling pathway in TNF-alpha/IFN-gamma-stimulated HaCaT cells. The oral administration of LM at 5 or 10 mu g/kg/day significantly reduced skin lesions, epidermal thickness, and mast cell infiltration in AD mice. Furthermore, LM reduced the production of IgE and inflammatory cytokines (TNF-alpha, IL-6, and IL-1 beta) in the serum, modulated gut microbiota diversity, and restored the microbial composition. Overall, our findings suggest that LM represents a potential therapeutic agent for improving AD symptoms through its ability to suppress inflammatory cytokines and alter the composition of gut microbiota.

Automated summary

The study investigated the therapeutic benefits of lipid mediators in atopic dermatitis (AD) and found that the mediators effectively reduced the production of inflammatory cytokines, inhibited the NF-kappa B signaling pathway, and altered the composition of gut microbiota. The results suggest that lipid mediators could be a potential therapeutic agent for improving AD symptoms.