Cyclooxygenase-2 (COX-2)-mediated prostaglandin E2 (PGE2) plays a key role in development and progression of inflammatory responses and Porphyromonas gingivalis is a common endodontic pathogen. In this study, we investigated induction of COX-2 and PGE2 by P. gingivalis in human dental pulp cells (HDPCs). P. gingivalis increased expression of COX-2, but not that of COX-1. Increased levels of PGE2 were released from P. gingivalis-infected HDPCs and this PGE2 increase was blocked by celecoxib, a selective COX-2 inhibitor. P. gingivalis activated all three types of mitogen-activated protein kinases (MAPKs). P. gingivalis-induced activation of nuclear factor-κB (NF-κB) was demonstrated by the results of phosphorylation of NF-κ B p65 and degradation of inhibitor of κB-α (IκB-α). Pharmacological inhibition of each of the three types of MAPKs and NF-κB substantially attenuated P. gingivalisinduced PGE2 production. These results suggest that P. gingivalis should promote endodontic inflammation by stimulating dental pulp cells to produce PGE2.

Introduction
 Materials and Methods
  Reagents
  Bacterial culture
  HDPCs culture
  RT-PCR
  ELISA
  Western blot
  Statistical analysis
 Results
  Induction of COX-2 mRNA expression
  Production of PGE2
  Activation of MAPKs and NF-κB pathways
  Effects of various signaling inhibitors
 Discussion
 Acknowledgments
 Conflict of interest
 References

• So-Hee Kim(Department of Oral Microbiology, School of Dentistry, Chonnam National University)
• Yun-Woong Paek(Department of Physical Therapy, Gwangju Health University)
• In-Chol Kang(Department of Oral Microbiology, School of Dentistry, Chonnam National University) Correspondence to