Abstract
Atopic dermatitis (AD) is an inflammatory skin disease characterized by intense pruritus and relapsable eczematous lesions. The hallmarks of AD are defects in the epidermal barrier and immunoglobulin E (IgE)-mediated sensitization to several environmental allergens, as well as an immune disorder mediated by an imbalance toward T-helper-2 response. Melittin, a major component of bee venom, has been studied in various inflammatory diseases. However, the beneficial effects of melittin on mouse with AD-like symptoms have not been explored. Therefore, we investigated the anti-allergic effects of melittin. AD was induced by ovalbumin (OVA) patch. After agent treatment, skin tissues and sera were extracted from the sacrificed mice were used to demonstrate the effects of melittin through various molecular biological methods. The results showed that OVA-induced skin thickening and inflammatory infiltration were decreased in the melittin-treated group. Melittin prevented OVA-induced filaggrin deficiency and imbalanced inflammatory mediators. Furthermore, melittin inhibited IL-4/IL-13-induced filaggrin downregulation through the blockade of STAT3 activation in human keratinocytes. In summary, this study has shown that melittin ameliorated OVA-induced AD-like symptoms from various perspectives. The findings of this study may be the first evidence of the anti-inflammatory effects of melittin on OVA-induced AD.
Highlights
Atopic dermatitis (AD) is an inflammatory skin disease characterized by intense pruritus and relapsable eczematous lesions
After AD induction, the skin conditions of the mice seemed to have worsened such as edema, erythema, and excoriation in the OVA group, but they were improved in the melittin group. (Fig. 1b)
AD is a chronic skin disease characterized by pruritus and eczematous skin lesions, accompanied by immune responses dominated with Th2 cells in the acute phase, defects in the epidermal barrier, a thickened epidermis, and immunoglobulin E (IgE)-mediated sensitization to several antigens[1]
Summary
Atopic dermatitis (AD) is an inflammatory skin disease characterized by intense pruritus and relapsable eczematous lesions It increases the risk for food allergy, asthma, allergic rhinitis, other immune-mediated diseases, and mental disorders[1]. The primary events and key drivers of AD are topics of continuing argument[4] Both hypotheses point out defects in the epidermal barrier and the immune system; the skin barrier function and the immune system closely interact. An increase in filaggrin expression may have a crucial role in the amelioration of the stratum corneum, and it may contribute to the recovery of the skin barrier function and to cutaneous inflammation. Disruptions in the epidermal barrier activate keratinocytes to produce chemokines that attract T cells, cytokines that mediate innate immune reactions (such as interleukin (IL)-1 family), and cytokines that trigger Th2 polarization and Langerhans cell activation (such as TSLP)[20]. A decrease in the expressions of TSLP and IL-13 is crucial to ameliorate pruritus in AD
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