Background and objectives
Porphyromonas gingivalis (P.
gingivalis) is regarded as a significant contributor in the
pathogenesis of periodontitis and certain systemic diseases, including
atherosclerosis. P. gingivalis occasionally translocates
from periodontal pockets into the circulation, where it adheres to red blood
cells (RBCs). This may protect the bacterium from contact with circulating
phagocytes without affecting its viability.
Materials and methods
In this in vitro study, we investigated whether
human peripheral blood neutrophils from 10 subjects with localized
aggressive periodontitis (LAgP) and ten healthy controls release the
pro-inflammatory cytokines interleukin (IL)-6, tumor necrosis factor
α (TNF-α), the chemokine (C-X-C motif) ligand 8 (CXCL8; also
known as IL-8) and chemokine (C-C motif) ligand 2 (CCL2; also known as
monocyte chemotactic protein (MCP)-1), and intracellular reactive oxygen
species (ROS) in response to challenge with P. gingivalis.
In addition, the impact of RBC interaction with P.
gingivalis was investigated. The actions of resolvin E1 (RvE1),
a known regulator of P. gingivalis induced neutrophil
responses, on the cytokine and ROS responses elicited by P.
gingivalis in cultures of neutrophils were investigated.
Results
Upon stimulation with P. gingivalis, neutrophils
from subjects with LAgP and healthy controls released similar quantities of
IL-6, TNF-α, CXCL8, CCL2 and intracellular ROS. The presence of RBCs
amplified the release of IL-6, TNF-α and CCL2 statistically
significant in both groups, but reduced the generation of ROS in the group
of healthy controls, and showed a similar tendency in the group of subjects
with LAgP. RvE1 had no impact on the production of intracellular ROS,
TNF-α, IL-6, CXCL8 and CCL2 by neutrophils from either group, but
tended to reduce the generation of ROS in subjects with LAgP in absence of
RBCs.
Conclusions
Our data support that binding to RBCs protects P.
gingivalis from ROS and concomitantly enhances neutrophil
release of pro-inflammatory cytokines providing a selective advantage for
P. gingivalis growth.