Abstract
IL-31 is a recently discovered cytokine that is produced not only in T-cells but also in mast cells. It is strongly implicated to play a key role in inflammatory diseases and in the pathogenesis of itch in atopic dermatitis. Apigenin, a flavonoid of plant origin has numerous biological applications. In this study, we showed that apigenin modulates IL-31 mRNA, protein expression, and release in stimulated human mast (HMC-1) by inhibiting the phosphorylation activation of MAPK and NF-κB. To determine whether apigenin has similar effects in vivo, using Compound 48/80, we developed an atopic dermatitis itch model in mice and found an increase in IL-31 expression in the skin. We also revealed that apigenin prevents the infiltration and degranulation of mast cells and suppressed mRNA and protein expression of IL-31 in the skin of mice. These results provide a new suggestion of the potential applicability of apigenin for treatment of various inflammatory diseases and itch mediated by IL-31.
Highlights
IL-31 is a recently discovered helical inflammatory cytokine that is derived from the gp130/IL-6 cytokine family, which consists of other cytokines such as IL-6 [1]
When the HMC-1 cells were treated with apigenin at either 10 μM, 20 μM, or 30 μM concentrations before stimulated with PI at indicated time intervals, a significant decrease of IL-31 release into the culture medium was observed with apigenin 20 μM and 30 μM
In an in vivo case study, we evaluated the anti-itch effect of apigenin in an atopic dermatitis itch model induced by compound 48/80
Summary
IL-31 is a recently discovered helical inflammatory cytokine that is derived from the gp130/IL-6 cytokine family, which consists of other cytokines such as IL-6 [1]. Its mRNA was first discovered in activated CD4+ T cells [1]. The mRNA has been found in activated mast cells [2]. IL-31 is known to play a key role in inflammatory diseases. Zhang et al (2008) found that IL-31 levels were elevated in skin biopsies of patients with atopic dermatitis compared to patients without atopic dermatitis [3]. The study found that IL-31 induced CCL1, CCL17, and CCL22 chemokines in atopic dermatitis-irritated skin. IL-31 was found to play a significant role in pruritus (itch) in atopic dermatitis. IL-31 mRNA was expressed in a mouse model of atopic dermatitis experiencing pruritus than in mice model of atopic dermatitis not experiencing pruritus [4]
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