Piper nigrum Fruit Extract Prevents TMA-Induced Allergic Contact Dermatitis by Regulating Th2 Cytokine Production

Sung Keun Jung,Chang Hwa Jung,Sun Young Jung,Dae Woon Choi,Yang-Ji Kim,Dong-Hwa Shon

doi:10.5539/jas.v7n2p135

Sung Keun Jung, Chang Hwa Jung + Show 4 more

Open Access

https://doi.org/10.5539/jas.v7n2p135

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Abstract

Allergic contact dermatitis (ACD) remains a leading skin disease in many countries. In this study, we investigated the preventive effect of Piper nigrum fruit extract (PFE) on trimellitic anhydride (TMA)-induced dermatitis and its potential mechanism of action. Oral administration of PFE and prednisolone (PS) significantly suppressed TMA-induced increases in ear, epidermal thickness, and infiltration of CD4+ cells, while abnormal expression of IgE, mMCP-1, IL-1B and IL-1B mRNA was also significantly counteracted by oral administration of PFE. PFE also significantly suppresses TMA-induced IL-4 and IL-5 production and IL-4 mRNA expression in vivo, as well as OVA-induced IL-4, IL-5, and IL-13 production and GATA3 mRNA expression ex vivo, and IL-4 induced STAT6 phosphorylation in primary cultured splenocytes and HaCaT cells. Interestingly, the PFE component piperine significantly suppressed OVA-induced IL-4, IL-5, and IL-13 secretion ex vivo. Taken together, these results suggest that PFE could be useful in suppressing allergic contact dermatitis.

Highlights

Allergic contact dermatitis (ACD) arises from a delayed type IV hypersensitivity response and is one of the most common skin diseases, affecting 15-20% of the general population worldwide (Peiser et al, 2012)
We investigated the preventive effect of Piper nigrum fruit extract (PFE) on trimellitic anhydride (TMA)-induced dermatitis and its potential mechanism of action
We investigated the preventive effect of Piper nigrum fruit extract on TMA-induced dermatitis using a murine ACD model

Summary

Introduction

Allergic contact dermatitis (ACD) arises from a delayed type IV hypersensitivity response and is one of the most common skin diseases, affecting 15-20% of the general population worldwide (Peiser et al, 2012). The generation of immunogenic neo-antigens occurs via binding between self-proteins and hapten compounds, as well as hapten and hapten-protein complexes recognized by the innate immune system as ‘altered self’, leading to the induction of several pro-inflammatory mediators, including interleukin-1β (IL-1β) (Kaplan et al, 2012). Following these events, haptenated skin-resident dendritic cells (DCs) or DCs with acquired haptenated proteins migrate to skin-draining lymph nodes, and peptides from haptenated cytokines act as signaling transducers which activate the signal transducer and activator of transcription (STAT), subsequently regulating T cell differentiation. Treg cells play a critical role in the regulation of immune cell homeostasis by producing IL-10 and transforming growth factor-beta (TGF-β) (Kim et al, 2013)

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