Porphorymonas gingivalis induces intracellular adhesion molecule-1 expression in endothelial cells through the nuclear factor-kappaB pathway, but not through the p38 MAPK pathway.

BACKGROUND AND OBJECTIVE

Porphyromonas gingivalis is a major pathogen in the development and progression of periodontal disease. The aim of this study was to investigate whether endothelial intracellular adhesion molecule-1 (ICAM-1), an inflammation biomarker for periodontitis, could be modified by infection with either of two strains of P. gingivalis with different virulence capacities: avirulent ATCC 33277 and virulent W83.

MATERIAL AND METHODS

We examined the expression of ICAM-1, IκBα, phospho-p38 MAPK and nuclear factor-kappaB (NF-κB) p65 in an umbilical vein endothelial cell line (ECV-304) treated with ATCC 33277 and W83, with or without the NF-κB antagonist MG132 and/or a specific p38 inhibitor (SB203580), by real-time PCR, western blotting and immunofluorescence.

RESULTS

Both strains could induce ICAM-1 expression; additionally W83 was able to increase ICAM-1 expression more significantly than ATCC 33277. In P. gingivalis-infected endothelial cells, both p38 MAPK and NF-κB signaling pathways were triggered by a rapid increase of p38 MAPK phosphorylation and a more delayed degradation of IκBα, followed by the nuclear translocation of NF-κB. It was found that ICAM-1 production in endothelial cells was abrogated by inhibition of the NF-κB pathway, but not by inhibition of the p38 MAPK pathway, using the inhibitors of the latter two molecules.

CONCLUSION

The induction of ICAM-1 by infection of umbilical vein endothelial cells with P. gingivalis might be mediated through the NF-κB pathway, but not by the p38 MAPK pathway.