Effect of myrrh oil on IL-1β stimulation of NF-κB activation and PGE2 production in human gingival fibroblasts and epithelial cells

Anecdotal and scientific evidence suggest that myrrh oil (MO) has anti-inflammatory properties. Subtoxic MO levels decrease interleukin (IL)-1 beta-stimulated production of the inflammatory cytokine IL-6 by human gingival fibroblasts, but not epithelial cells. IL-1 beta upregulates IL-6 via PGE(2), and via NF-kappa B, a transcription factor for many inflammatory mediator genes. NF-kappa B is inhibited by sesquiterpene compounds (from plants other than myrrh). This study determined MO effect on IL-1 beta-stimulated PGE(2) production and NF-kappa B activation in gingival fibroblasts and epithelial cells. Cells were preincubated with MO, exposed to IL-1 beta, cytoplasmic and nuclear fractions were isolated, and activated NF-kappa B was measured using an ELISA-based assay. IL-1 beta increased nuclear activated NF-kappa B levels in fibroblasts and epithelial cells [10- and 2.5-fold over controls, respectively (p = 0.0001)], and these increases were not significantly affected by MO. PGE(2) was measured in cell supernatants by ELISA, after preincubation with MO and exposure to IL-1 beta. MO inhibited IL-1 beta-stimulated PGE(2) production by fibroblasts (p = 0.00 1), but not epithelial cells. The data suggest that gingival epithelial cells and fibroblasts may differ in the magnitude of NF-kappa B activation after IL- 10 stimulation, and that MO inhibition of IL-1 beta-stimulated IL-6 production in fibroblasts is due in part to inhibition of PGE(2), but not NF-kappa B activation. (Supported by NIDCR DE-0725.) (c) 2005 Elsevier Ltd. All rights reserved.