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E‐selectin expression induced by P orphyromonas gingivalis in human endothelial cells via nucleotide‐binding oligomerization domain‐like receptors and Toll‐like receptors
Author(s) -
Wan M.,
Liu J.R.,
Wu D.,
Chi X.P.,
Ouyang X.Y.
Publication year - 2015
Publication title -
molecular oral microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.18
H-Index - 77
eISSN - 2041-1014
pISSN - 2041-1006
DOI - 10.1111/omi.12102
Subject(s) - receptor , microbiology and biotechnology , chemistry , biology , biochemistry
Summary P orphyromonas gingivalis , an important periodontal pathogen, has been proved to actively invade cells, induce endothelial cell activation, and promote development of atherosclerosis. Innate immune surveillance, which includes the activity of nucleotide‐binding oligomerization domain ( NOD )‐like receptors ( NLR s) and Toll‐like receptors ( TLR s), are essential for the control of microbial infections; however, the roles of receptor families in P . gingivalis infections remain unclear. Here, we examined the roles of NLR s and TLR s in endothelial cell activation caused by P . gingivalis . Live P . gingivalis and whole cell sonicates were used to stimulate endothelial cells, and both showed upregulation of E‐selectin as well as NOD 1, NOD 2, and TLR 2. In addition, silencing of these genes in endothelial cells infected with P . gingivalis led to a reduction in E‐selectin expression. P orphyromonas gingivalis also induced nuclear factor‐κB ( NF ‐κB) and P38 mitogen‐activated protein kinase ( MAPK ) activity in endothelial cells, whereas small interfering RNA targeting NOD 1 significantly reduced these signals. Moreover, inhibition of either NOD 2 or TLR 2 inhibited NF ‐κB significantly, but had only a weak inhibitory effect on P38 MAPK signaling. Direct inhibition of NF ‐κB and P38 MAPK significantly attenuated E‐selectin expression induced by P . gingivalis in endothelial cells. Taken together, these findings suggest that NOD 1, NOD 2, and TLR 2 play important, non‐redundant roles in endothelial cell activation following P . gingivalis infection.