Abstract
Fucoxanthin (FX) is a xanthophyll that is contained abundantly in marine plants. The biological action of FX includes its antioxidant and anti-lipogenic activities, while the precise action of its mechanisms on skin cells has not yet been clarified. The current study examined the effect of FX in comparison with tacrolimus (TAC) on NC/Nga mice, which are an atopic dermatitis (AD) model. FX topical treatment dramatically ameliorated itching behavior over the TAC treatment, which was insufficient for improvement of AD symptoms. In Nc/Nga mice, FX or TAC applied to the skin inhibited eosinophil infiltration with decreased expression of Il-33. FX also stimulated Il-2, Il-5, Il-13, Il-10, and TGF-β expression levels, and Sca1+Il-10+TGF-β+ regulatory innate lymphoid cells (ILCreg) were dominantly observed in FX treated skin epidermal keratinocytes and dermal layers. This combined evidence demonstrated that FX exerts anti-inflammatory effects on keratinocytes and ameliorates AD symptoms by regulating ILCreg to normalize immune responses in an atopic dermatitis model.
Highlights
Atopic dermatitis (AD), which affects at least 15% of children in developed countries, causes dry, scaly, and itchy skin [1]
TAC had no effect on the expression of ILCreg-derived anti-inflammatory cytokines such as Il-2 and Il-10
We report here that FX brought about a dramatic improvement in AD symptoms by regulating ILCreg
Summary
Atopic dermatitis (AD), which affects at least 15% of children in developed countries, causes dry, scaly, and itchy skin [1]. Elevated IgE causes degranulation by binding to a high-affinity receptor FcεRI expressed on mast cells, resulting in itching in allergic diseases [6,7]. Mast cell function is regulated indirectly by non-mast cells, including adaptive helper T cells [6,9]. Compounds that modulate mast cells and adaptive helper T cells would require a systematic reassessment of immune function. Apart from the lipid metabolism, several carotenoids inhibit the degranulation of mast cells by suppressing the antigen-induced aggregation of the high affinity IgE receptor (Fc RI) in vitro [18,19]. FX temporarily suppressed mast cell-dependent scratching behavior These effects were common with TAC and contributed to improving AD symptoms. TAC had no effect on the expression of ILCreg-derived anti-inflammatory cytokines such as Il-2 and Il-10. We report here that FX brought about a dramatic improvement in AD symptoms by regulating ILCreg
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