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Br J Pharmacol. 2018 Dec;175(23):4310-4324. doi: 10.1111/bph.14487. Epub 2018 Nov 6.

Therapeutic effects of bee venom and its major component, melittin, on atopic dermatitis in vivo and in vitro.

Author information

1
Department of Pathology, College of Medicine, Catholic University of Daegu, Daegu, Korea.
2
Department of Agricultural Biology, National Academy of Agricultural Science, Jeonju-si, Korea.
3
School of Biomedical Sciences, Charles Sturt University, Bathurst, NSW, Australia.
4
Department of Immunology, College of Medicine, Catholic University of Daegu, Daegu, Korea.
5
Department of Oral and Maxillofacial Surgery, Department of Dentistry, College of Medicine, Catholic University of Daegu, Daegu, Korea.

Abstract

BACKGROUND AND PURPOSE:

Atopic dermatitis (AD) is a multifactorial skin condition with complex interactions of innate and adaptive immune responses. There are several existing therapies for AD, including topical glucocorticosteroids, emollients, phototherapies, calcineurin inhibitors and immunosuppressants, such as cyclosporine A. Although these therapies reduce inflammation, they also cause serious side effects. Therefore, it is necessary to develop new therapeutic approaches for AD treatment without side effects. There are several studies on natural materials or toxins, such as herbs, ginseng extract and snake venom, for AD treatment. However, treatment of AD with bee venom and its major component, melittin has rarely been studied.

EXPERIMENTAL APPROACH:

Effects of bee venom and melittin were studied in a model of AD in vivo induced by 1-chloro-2,4-dinitrobenzene (DNCB) in female Balb/c mice and in cultures of human keratinocytes, stimulated by TNF-α/IFN-γ. The potential pharmacological effects of bee venom and melittin on these in vivo and in vitro AD-like skin disease models were studied.

KEY RESULTS:

Bee venom and melittin exhibited potent anti-atopic activities, shown by decreased AD-like skin lesions, induced by DNCB in mice. In vitro studies using TNF-α/IFN-γ-stimulated human keratinocytes showed that bee venom and melittin inhibited the increased expression of chemokines, such as CCL17 and CCL22, and pro-inflammatory cytokines, including IL-1β, IL-6 and IFN-γ, through the blockade of the NF-κB and STAT signalling pathways.

CONCLUSIONS AND IMPLICATIONS:

Our results suggest that bee venom and melittin would be suitable for epicutaneous application, as topical administration is often appropriate for the treatment of AD.

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