Bee Venom Helps Treat Atopic Dermatitis (Eczema)

Use of Bee Venom for Topical Treatment in Patients With Atopic Dermatitis

Dermatology Advisor

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The use of bee venom (BV) and its major component, melittin, has proven suitable as an epicutaneous application for the treatment of atopic dermatitis (AD), according to the results of an in vivo and in vitro study conducted in an AD-like model, with findings published in the British Journal of Pharmacology.

The investigators sought to explore the potential pharmacologic effects of bee venom and melittin on 1-chloro-2,4-dinitrobenzene (DNCB)-induced in vivo and tumor necrosis factor-alpha (TNF-α)/tumor necrosis factor-gamma (TNF-γ) in vitro AD-like models of skin disease.

Study results showed that bee venom and melittin possess potent anti-atopic activities, as demonstrated by decreased DNCB-induced AD-like skin lesions in an animal model. In vitro studies that used TNF-α/ TNF-γ–stimulated human keratinocytes revealed that bee venom and melittin inhibit the exaggerated expression of such chemokines as TARC/CCL17 and MDC/CCL22, as well as such pro-inflammatory cytokines as interleukin-1-beta (IL-1β), IL-6, and interferon (IFN)-γ, via blockade of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and signal transducers and activators of transcription (STAT) pathways.

The investigators concluded that since the use of topical agents is often recommended for the treatment of AD, bee venom and melittin are suitable for epicutaneous application. The results of this study showed the ameliorating effects of bee venom and melittin on the DNBC-induced AD-like skin lesions in BALB/c mice and TNF-α/ TNF-γ–stimulated human keratinocyte HaCaT cells.

By suppressing production of Th1/Th2–associated and pro-inflammatory cytokines, bee venom and melittin decreased inflammatory symptoms in AD-like skin lesions, resulting in a subsequent reduction in CD4+ T cells, mast cell infiltration, and release of serum immunoglobulin E (IgE). Moreover, bee venom and melittin improved abnormal epidermal differentiation by restoration of filaggrin expression.