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

Prostaglandin F2alpha (PGF2α) and interleukin-1beta (IL-1β) levels are elevated in inflamed dental pulp. The roles of IL-1β and PGF2α in the pathogenesis of pulpal inflammation await investigation. We found that IL-1β stimulated PGF2α production of human dental pulp cells. IL-1β and PGF2α (0.5–10 μmol/L) also induced IL-8 production and mRNA expression in pulp cells. Aspirin inhibited IL-1β–induced PGF2α, but not IL-8 production. PGF2α-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-1β–induced IL-8 production in pulp cells is not mainly via direct activation of cyclooxygenase and PGF2α generation. PGF2α-induced IL-8 production is possibly via activation of MEK/extracellular signal-regulated kinase signaling, but not by activation of adenylate cyclase. IL-1β and PGF2α might involve the pathogenesis of pulpal inflammation via induction of IL-8 production.