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Innate Immunity
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Article

PLC, p38/MAPK, and NF{kappa} B-mediated induction of MIP-3{alpha}/CCL20 by porphyromonas gingivalis

Henrik Dommisch*, Whasun O Chung, Søren Jepsen, Beth M Hacker, and Beverly A Dale

University Hospital Bonn

* To whom correspondence should be addressed. E-mail: dommisch{at}uni-bonn.de.


  Abstract

Macrophage inflammatory protein-3{alpha}/C-C chemokine ligand 20 (MIP-3{alpha}/CCL20) is an antimicrobial peptide that plays an important role in innate immunity. In addition to direct microbicidal effects, MIP-3{alpha}/CCL20 also exhibits cytokine-like functions that are critical during dendritic cell activation. The aim of the present study was to investigate further which signaling pathways are involved in the MIP-3{alpha}/CCL20 mRNA expression in response to whole-cell Porphyromonas gingivalis. Primary gingival epithelial cells (GECs) and the immortalized oral keratinocyte cell-line OKF6/TERT-2 were stimulated with whole-cell P. gingivalis. Prior to stimulation, GECs and OKF6/TERT-2 cells were pretreated with specific inhibitors for nuclear-factor-{kappa}B (NF-{kappa}B), mitogen-activated protein kinase (MAPK), phospholipase C (PLC), and phosphatidylinositol-3-kinase (PI3K). In GECs and OKF6/TERT-2 cells, activation of NF-{kappa}B was examined after exposure to P. gingivalis. The gene expression of MIP-3{alpha}/CCL20 was significantly induced in response to P. gingivalis (P ≤ 0.05) compared to unstimulated control cells. This induction was specifically blocked when cells were pre-incubated with inhibitors for NF-{kappa}B, MAPK, and PLC (P ≤ 0.05), but not for PI3K. These results demonstrate that P. gingivalis induces the MIP-3{alpha}/CCL20 mRNA in a NF-{kappa}B-, PLC-, and MAPK-dependent manner.

First published on August 26, 2009
Innate Immunity 2009, doi:10.1177/1753425909339237
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