Neutrophils |
PAR-2 Rgp |
Increase in the intracellular Ca2+ concentration |
Neutrophil activation |
(112) |
Osteoblasts |
PAR-2 Rgp |
Increase in the intracellular Ca2+ concentration |
Activation of osteoblast-mediated osteoclastic bone resorption |
(2) |
Platelets |
PAR-1, -4 RgpA, RgpB |
Platelets aggregation |
A putative link between periodontitis and cardiovascular disease |
(114) |
Oral epithelial cells |
PAR-1, -2 |
Stimulation of interleukin-6 expression |
Inflammatory events associated with periodontal disease |
(113) |
Platelets |
PARs Rgp enriched vesicles |
Platelets aggregation |
As above |
(166) |
Pulp cells |
PAR-2 RgpB |
Induced expression of neuropeptides: calcitonin gene-related peptide (CGRP) and substance P (SP) |
A putative link between periodontitis and pulp inflammation |
(217) |
Gingival fibroblasts |
PAR-1, -2 Rgp |
Induced expression of hepatocyte growth factor |
Effect on both inflammatory and tissue reparative processes |
(220) |
Rat kidney epithelial cells |
PAR-2 P. gingivalis culture supernatants |
Ca2+ mobilization |
|
(61) |
Keratinocytes |
PAR-1, -2 Rgp |
Up-regulation of HIV-1 co receptor CCR5 |
Promotion of HIV infection of oral keratinocytes |
(43) |
Oral epithelial cells |
PAR-2 Rgp |
Induced expression of human β-defensins-2 and CC chemokine ligand 20 (CCL20) |
Enhancement of mucosal antibacterial defense |
(31) |
T cells |
PAR-1, -2, -4 RgpA |
Induced expression of CD25 and CD65 |
T cell activation |
(237) |
Vascular endothelial cells |
PAR RgpA |
Weibel-Palade body exocytosis, enhanced production of interleukin-8 in response to lipopolysaccharide |
Enhanced proinflammatory responses to P. gingivalis
|
(76) |
Oral epithelial cells |
PAR-1, -2 Rgp, Kgp |
RgpB upregulate while Kgp and RgpA downregulate interleukin-8 expression |
Attenuation of neutrophils migration and sustained chronic inflammation |
(221) |
Monocytic THP-1 cells |
PARs Rgp, Kgp |
Up-regulation of pro-inflammatory cytokines (interleukin-6, interleukin-8 and monocyte chemoattractant protein-1) |
Synergistic effect of PAR-dependent and PAMPs receptor (Toll-like receptors or NOD1/2) signaling resulting in enhancement of mucosal antibacterial defense |
(219) |
ST2 mouse stromal cells and calvarial osteoblasts |
PAR P. gingivalis cells |
Proinflammatory responses independent of the Toll-like receptor/MyD88 pathway |
Pathogen recognition: enhancement of mucosal antibacterial defense |
(148) |
Platelets |
PARs Rgps |
Platelet sensitization to aggregation by the stress hormone epinephrine |
Mechanistic explanation of a direct connection between periodontitis and stress |
(139) |
Human oral keretinocytes |
PAR-1, -2 P. gingivalis cells |
PAR-1 cleavage by Rgps mediated up-regulation of pro-inflammatory cytokines (interleukin-1α, interleukin-1β, interleukin-6, tumor necrosis factor-α) |
Osteoclasts differentiation and alveolar bone resorption |
(42) |