Prostaglandin F2α-Induced Interleukin-8 Production in Human Dental Pulp Cells Is Associated With MEK/ERK Signaling

Prostaglandin F-2alpha (PGF(2 alpha)) and interleukin-1 beta (IL-1 beta) levels are elevated in inflamed dental pulp. The roles of IL-1 beta and PGF(2 alpha) in the pathogenesis of pulpal inflammation await investigation. We found that IL-1 beta stimulated PGF(2 alpha) production of human dental pulp cells. IL-1 beta and PGF(2 alpha) (0.5-10 mu mol/L) also induced IL-8 production and mRNA expression in pulp cells. Aspirin inhibited IL-1 beta-induced PGF(2 alpha) but not IL-8 production. PGF(2 alpha)-induced IL-8 production and mRNA expression were inhibited by U0126 (an inhibitor of mitogen-activated protein kinase kinase [MEK1/2]) inhibitor), whereas SQ22536 (an adenylate cyclase inhibitor) enhanced this event. These results indicate that IL-1 beta-induced IL-8 production in pulp cells is not mainly via direct activation of cyclooxygenase and PGF(2 alpha) generation. PGF(2 alpha)-induced IL-8 production is possibly via activation of MEK/extracellular signal-regulated kinase signaling, but not by activation of adenylate cyclase. IL-1 beta and PGF(2 alpha) might involve the pathogenesis of pulpal inflammation via induction of IL-8 production. (J Endod2009;35:508-512)