Conclusion
The Results reveal the important role of IL-1β in pulpal inflammatory responses via stimulation of IL-8 and ICAM-1 expression and secretion. Moreover, IL-1β-induced effects on IL-8 and ICAM-1 are differentially regulated by IRAK1/4 and p38 signaling in dental pulp cells. Blocking of IRAKs and p38 signaling may have potential to control inflammation of dental pulp in the future.
Methods
Cultured human dental pulp cells were exposed to IL-1β with/without pretreatment and co-incubation with IRAK1/4 inhibitor or SB203580 (p38 inhibitor). IRAK-1 phosphorylation was evaluated by immunno fluorescent staining. The protein expression of ICAM-1 and IL-8 were tested by western blotting. The secretion of soluble ICAM-1 (sICAM-1) and IL-8 was measured by enzyme-linked immunosorbant assay (ELISA).
Purpose
Interleukin 1 beta (IL-1β) is a pro-inflammatory cytokine involved in the acute and chronic inflammatory processes of dental pulp. Intercellular adhesion molecule-1 (ICAM-1) and IL-8 are two major inflammatory mediators. However, the role of interleukin-1 receptor-associated kinases (IRAKs) signaling pathways in responsible for the inflammatory effects of IL-1β on dental pulp cells is not clear.
Results
IL-1β stimulated IRAK-1 phosphorylation of pulp cells within 120 min of exposure. IRAK1/4 inhibitor attenuated the IL-1β-induced ICAM-1, but not IL-8 protein expression. IRAK1/4 inhibitor also prevented the IL-1β-induced sICAM-1, but not IL-8 secretion. SB203580 showed little effect on IL-1β-induced sICAM-1 secretion, but effectively inhibited its induction of IL-8 secretion in pulp cells.