Abstract

Morinda citrifolia, a fruit generally known as “Noni”, has been traditionally used in parts of East Asia to relieve inflammatory diseases. Although several studies using noni have been reported, the effect of fermented Morinda citrifolia (F.NONI) on atopic dermatitis (AD) has not been investigated. Thus, we aimed to investigate the improving effect of F.NONI treatment on AD-like skin lesions and elucidate molecular mechanisms. F.NONI was prepared by the fermentation of noni fruit with probiotics and then extracted. F.NONI was orally administrated to NC/Nga mice to evaluate its therapeutic effect on 2,4-dinitrochlorobenzene (DNCB)-induced AD. Oral administration of F.NONI significantly alleviated AD lesions and symptoms such as dermatitis scores, ear thickness, scratching behavior, epidermal thickness, and infiltration of inflammatory cells (e.g., mast cells and eosinophils). In addition, F.NONI treatment reduced the levels of histamine, IgE and IgG1/IgG2a ratio, thymus and activation regulated chemokine (TARC), and thymic stromal lymphopoietin (TSLP) in serum and beneficially modulated the expressions of Th1, Th2, Th17, and Th22-mediated cytokines in lesioned skin and splenocytes. Furthermore, the expressions of the skin barrier-related proteins including filaggrin (FLG), loricrin (LOR), involucrin (IVL), zonula occludens-1 (ZO-1), and occludin (OCC) were restored by F.NONI treatment. Taken together, these results suggest that F.NONI could be a therapeutic agent to attenuate AD-like skin lesions through modulating the immune balance and skin barrier function.

Highlights

  • Atopic dermatitis (AD) is a multifactorial, chronic inflammatory skin disorder accompanied by pruritus, dry skin, abnormal immune responses, and impaired epidermal barrier, which has no influence on normal, non-atopic individuals [1]

  • We investigated the protective effects of fermented Morinda citrifolia (F.NONI) in a DNCB-induced atopic dermatitis model in vivo

  • This study focused on the AD-like skin lesion symptoms and the immunological balance of Th1 and Th2, and skin barrier function involved in tight junction (TJ) proteins

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Summary

Introduction

Atopic dermatitis (AD) is a multifactorial, chronic inflammatory skin disorder accompanied by pruritus, dry skin, abnormal immune responses, and impaired epidermal barrier, which has no influence on normal, non-atopic individuals [1]. Compromised skin barrier integrity allows entry of external antigens and allergens, which activate immune responses across the skin surface. Under such conditions, pro-inflammatory cytokines including IL-6, IL-33, TNF-α, and thymic stromal lymphopoietin (TSLP) are produced by keratinocytes and Langerhans cells (LCs) [8]. Pro-inflammatory cytokines including IL-6, IL-33, TNF-α, and thymic stromal lymphopoietin (TSLP) are produced by keratinocytes and Langerhans cells (LCs) [8]

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