Premium
Nuclear factor‐κB p50 subunits in chronic periodontitis and Porphyromonas gingivalis lipopolysaccharide‐pulsed dendritic cells
Author(s) -
Jotwani Ravi,
Moonga Baljit S.,
Gupta Siddharth,
Cutler Christopher W.
Publication year - 2010
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.05247.x
Subject(s) - porphyromonas gingivalis , tlr4 , tlr2 , lipopolysaccharide , chronic periodontitis , toll like receptor , chemistry , microbiology and biotechnology , dendritic cell , immunology , monocyte , cytokine , periodontitis , biology , inflammation , innate immune system , immune system , medicine
The pathogenesis of a number of chronic inflammatory diseases has been linked to dysregulated functioning of nuclear transcription factor (NF)‐κB. In the present study, we examine NF‐κB activation in human oral mucosal tissues of chronic periodontitis (CP) patients. Electrophoretic mobility shift assay and DNA‐binding enzyme‐linked immunosorbent assays indicate elevated levels of transcriptionally repressive p50 subunits and an increased p50/p65 ratio in CP tissues compared to healthy controls. Because Porphyromonas gingivalis has been recognized to be a causal factor in CP, we used P. gingivalis lipopolysaccharide (LPS) for in vitro studies with monocyte‐derived dendritic cells (MoDCs). Porphyromonas gingivalis LPS, unlike Escherichia coli LPS, induced an increased p50/p65 ratio in MoDCs. Using blocking antibodies, we demonstrated that while both Toll‐like receptor 2 (TLR2) and TLR4 are required for MoDC maturation by P. gingivalis LPS, only TLR4 signaling is sufficient to induce cytokine secretion. Our results suggest that increased levels of transcriptionally repressive p50 may be characteristic of CP and might be a result of suboptimal NF‐κB activation and dendritic cell maturation by P. gingivalis, a bacterium implicated in CP.