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Ability of Supragingival Plaque to Induce Toll‐Like Receptor 4–Mediated Stimulation Is Associated With Cytokine Production by Peripheral Blood Mononuclear Cells
Author(s) -
Yamaguchi Ryusuke,
Yoshimura Atsutoshi,
Yoshioka Hidenobu,
Kaneko Takashi,
Hara Yoshitaka
Publication year - 2009
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2009.080393
Subject(s) - tlr4 , tlr2 , cytokine , peripheral blood mononuclear cell , proinflammatory cytokine , stimulation , toll like receptor , tumor necrosis factor alpha , receptor , immunology , chemistry , medicine , inflammation , endocrinology , in vitro , innate immune system , biochemistry
Background: In our previous study, we found that the ability of supragingival plaque to induce Toll‐like receptor (TLR)4‐mediated stimulation was positively associated with plaque score and bleeding on probing (BOP) at the sampled sites and that the ability to induce TLR2‐mediated stimulation was negatively associated with probing depth (PD) and clinical attachment level (CAL). Because signaling from TLR leads to the induction of pro‐ and anti‐inflammatory cytokines, we further analyzed the influence of the ability of supragingival plaque to induce TLR2‐/TLR4‐mediated stimulation of cytokine production by peripheral blood mononuclear cells (PBMCs). Methods: The abilities of 125 plaque samples to induce TLR2‐ or TLR4‐mediated stimulation were determined using genetically engineered Chinese hamster ovary reporter cells that express a reporter molecule upon activation of nuclear factor‐kappa B through TLR2 or TLR4. PBMCs were stimulated with each plaque sample, and the production of proinflammatory cytokines (tumor necrosis factor‐alpha and interleukin [IL]‐6 and −8) and an anti‐inflammatory cytokine (IL‐10) was analyzed by enzyme‐linked immunosorbent assay. Results: The levels of the cytokines produced by PBMCs all correlated with the ability of supragingival plaque to induce TLR4‐mediated stimulation but not with its ability to induce TLR2‐mediated stimulation. Cytokine production was inhibited by an anti‐TLR4 monoclonal antibody and a TLR4 antagonist, compound 406. The levels of cytokines were associated with plaque index, BOP, PD, and CAL at the sampled sites. Conclusions: The production of pro‐/anti‐inflammatory cytokines by PBMCs was associated with the ability of supragingival plaque to induce TLR4‐mediated stimulation. The cytokines induced by supragingival plaque via TLR4 might modulate periodontal status.