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Apis Mellifera Venom and Melittin Block neither NF-B-p50-DNA Interactions nor the Activation of NF-B, Instead They Activate the Transcription of Proinflammatory Genes and the Release of Reactive Oxygen Intermediates¹

Ludwig Boltzmann Institute for Rheumatology and Balneology, Vienna, Austria

Many alternative treatment approaches, originating from Asia, are becoming increasingly popular in the Western hemisphere. Recently, an article published in a renowned journal reported that venom of apis mellifera (bee venom (BV)) and melittin mediate immune-modulating effects by blocking the activation of the transcription factor NF-B. Such a modus operandi would corroborate the many claims of beneficial effects of BV treatment and give immediate credit to this form of therapy. Fibroblast-like synoviocytes from rheumatoid arthritis patients and dermal fibroblast cells and white blood cells from healthy volunteers were used to study the effects of BV and melittin on the activation of NF-B and a series of genes that are markers of inflammation. EMSAs demonstrate that neither BV nor melittin blocked IL-1-induced NF-B activation; neither did they affect phosphorylation or degradation of IB. Contrary to published data, even high concentrations of BV and melittin were without any effect on NF-B-p50-DNA interactions. More importantly, in fibroblast-like synoviocytes, but also in dermal fibroblasts as well as in mononuclear cells exposed to BV or melittin, mRNA levels of several proinflammatory genes are significantly increased, and Western blot data show elevated cyclooxygenase-2 protein levels. Furthermore, exposure to BV higher than 10 µg/ml resulted in disintegration of all cell types tested. In addition, large quantities of oxygen radicals are produced in a dose-dependent manner in leukocytes exposed to BV. Taken together, data presented in this work do not corroborate an earlier report regarding the effectiveness of BV as an inhibitor of the transcription factor NF-B.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported in part by a grant from the Austrian National Bank.

² Address correspondence and reprint requests to Dr. Karl M. Stuhlmeier, Ludwig Boltzmann Institute for Rheumatology and Balneology, Kurbadstrasse 10, 1100 Vienna, Austria. E-mail address: karlms{at}excite.com

³ Abbreviations used in this paper: BV, bee venom; COX-2, cyclooxygenase-2; CT, threshold cycle; DCFH-DA, 2',7'-dichlorofluorescin-diacetate; FLS, fibroblast-like synoviocyte; HAS1, hyaluronansynthase-1; LC, loading control; MED, medium; MNC, mononuclear cell; PMN, polymorphonuclear cell; RFU, relative fluorescence unit; SF, dermal fibroblast cell.

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