Induction of Prostaglandin E₂ by Porphyromonas gingivalis in Human Dental Pulp Cells.
10.11620/IJOB.2017.42.4.149
- Author:
So Hee KIM
1
;
Yun Woong PAEK
;
In Chol KANG
Author Information
1. Department of Oral Microbiology, School of Dentistry, Chonnam National University, Gwangju, 61186, Republic of Korea. ickang@jnu.ac.kr
- Publication Type:Original Article
- Keywords:
Human dental pulp cells;
prostaglandin E₂;
cyclooxygenase-2;
Porphyromonas gingivalis
- MeSH:
Celecoxib;
Cyclooxygenase 2;
Dental Pulp*;
Dinoprostone;
Humans*;
Mitogen-Activated Protein Kinases;
Phosphorylation;
Porphyromonas gingivalis*;
Porphyromonas*;
Pulpitis
- From:International Journal of Oral Biology
2017;42(4):149-153
- CountryRepublic of Korea
- Language:English
-
Abstract:
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. gingivalis induced PGE2 production. These results suggest that P. gingivalis should promote endodontic inflammation by stimulating dental pulp cells to produce PGE₂.
